Practice nursing care for Clients

Practice nursing care for Clients

with Renal Disorders


  Renal problems: infectious disorders

 The urinary system is normally one in which a sterile body fluid (urine) is excreted. The unobstructed and complete passage of urine from the renal and urinary systems is critical to the steril­ity of the urinary tract. When a structural abnormality (either congenital or acquired) is present, the potential for degenerative changes from infection is dramatically increased. Urinary tract infection (UTI) usually refers to infections in this sterile sys­tem. Pyelonephritis is a bacterial infection within the kidney and renal pelvis—theupper urinary tract. Infections within the lower urinary tract are described in Chapter.



With improved diagnostic techniques and a better under­standing of the inflammatory response, pyelonephritis has come to refer to active microorganisms or the effects of kid­ney infections. Acute pyelonephritis is the condition result­ing from an active bacterial infection, whereas chronic pyelonephritis results from repeated or continued upper uri­nary tract infections or infectious sequelae. Chronic pyelonephritis is usually associated with an anatomic urinary tract anomaly, urinary obstruction or, most commonly,vesi-coureteral reflux. The vesicoureteral junction is the point at which the ureter joins the bladder. Reflux refers to the re­verse (e.g., backward, upward, ascending) flow of urine to­ward the renal pelvis and kidney.


In pyelonephritis, microorganisms usually ascend from the lower urinary tract into the renal pelvis. Infection from organisms carried in the blood (hematogenous) may occur, but mey occur with much less frequency. Bacteria activate the in-matoryresponse, and local edema results.

Acute pyelonephritis involves acute interstitial inflamma­tion, tubular cell necrosis, and a tendency for abscess forma­tion. Abscesses, pockets of localized infection, can appear in the capsule, cortex, or medulla. The pattern of infection within the kidney is not uniform; normal tissue and tubules can lie next to infected areas. Fibrosis or scar tissue develops as the inflammatory process subsides. The calices become blunted, and scars develop in the interstitial tissue.

Vesicoureteral and intrarenal reflux of infected urine are the major mechanisms responsible for chronic pyelonephritis. Some papillae in the kidney do not close with increased in-tracaliceal pressure, causing intrarenal reflux. Refluxing papillae are most often located in the upper and lower poles of the kidney and therefore are more susceptible to chronic pyelonephritis. Inflammation, fibrosis, and deformity of the renal pelvis and calices are evident. Repeated or continuous infectious produce additional scar tissue. Vascular, glomeru-lar, and tubular changes within the scars can occur. Filtration, reabsorption, and secretion are eventually impaired, and renal function is diminished (Figure 71-3).


Single episodes of acute pyelonephritis may result from the en­try of bacteria associated with pregnancy, obstruction, or reflux.Chronic pyelonephritis is usually associated with structural ab­normalities and/or obstruction with reflux. Vesicoureteral re­flux or obstruction leading to chronic pyelonephritis is often due to stones, obstruction, or neurogenic impairment involving the voiding mechanism. Reflux is more common in children, who as adults often have scarring associated with chronic pyelonephritis. Clients who develop chronic pyelonephritis without having reflux as a child are usually adults with a his­tory of spinal cord injury, bladder tumor, prostatic hypertrophy, or urinary tract stones.

Acute or chronic pyelonephritis is more likely to occur in clients who have undergone manipulation of the urinary tract (e.g., placement of a urinary catheter), those who have dia­betes mellitus or chronic renal calculi, or those who overuse analgesics. In clients with diabetes mellitus, the development and progression of bladder atony increase the tendency to de­velop pyelonephritis. In clients with chronic stone disease, j calculi provide a site for ongoing infection and resultant renal scarring. Nonsteroidal anti-inflammatory drug (NSAID) use has been associated with papillary necrosis, which then per- \ mits reflux.

The most common pyelonephritis-causing organism is Escherichia coli. Enterococcus faecalis is typical in hospital­ized clients. Both are organisms of the gastrointestinal tract. Non-£. coli organisms such as Proteus mirabilis, Klebsiella and Pseudomonasaeruginosa and the more antibiotic-resist­ant organisms are also causes of pyelonephritis in hospital­ized clients. When the infection is bloodborne, common in­fecting organisms include Staphylococcus aureus and the Candida and Salmonella species.

Theories of noninfectious or idiopathic causes of intrarenal scarring and the eventual outcome of pyelonephritis include an antibody reaction, cell-mediated immunity against the bac­terial antigens, or an autoimmune reaction.


The exact incidence and prevalence of pyelonephritis are not known; this diagnosis is not separately reported from all uri­nary tract infections. Acute urinary conditions of the kidneys or urinary tract, nephritic syndrome, urethral stricture, and cystitis account for more than 7 million new cases annually in noninstutionalized Americans (NIDDK National Kidney and Urologic Diseases Information Clearinghouse, 1999). Women overall have more cases of pyelonephritis. After age 65, rates for men increase greatly because of the increased incidence of prostatitis.




The nurse asks about a history of urinary tract infections (UTIs), diabetes mellitus, stone disease, and other structural or functional abnormalities of the genitourinary tract. The nurse attempts to determine whether the UTIs were associ­ated with pregnancy and asks the client about any previous experiences with pyelonephritis or similar symptoms. Recur­rences are common and may lead to a deterioration of renal function.


The nurse asks the client about specific symptoms associated with acute pyelonephritis. Chronic pyelonephritis has a less dramatic clinical presentation; signs and symptoms are usually related to the infection or renal function. The nurse asks the client to describe any vague or nonspecific urinary. The nurse advises the client to complete all prescribed an­tibiotic regimens and instructs the client to report any side ef­fects or unusual symptoms to the prescribing health team member rather than suspend the regimen. The client and fam­ily are referred for nutritional counseling as needed, because many clients have special nutritional requirements, such as those caused by diabetes mellitus or pregnancy.


If no surgery is performed, the client may need assistance with self-care, nutrition, and medication administration at home. If surgical intervention is necessary, the client may re­quire help with incision care, self-care, and transportation for follow-up medical appointments.


The client may also briefly need a community health nurse to help administer medications or nutrition at home. House­keeping services may also be helpful while the client is re­gaining strength.

• Evaluation: Outcomes

The nurse evaluates the care of the client with pyelonephri­tis on the basis of the identified nursing diagnoses and col­laborative problems. Expected outcomes may include that the client will:

  Demonstrate methods of enhancing comfort

  Report that pain is controlled

  Express satisfaction with pain control

  Describe the role of antibiotics and self-administration of medications

  Explain and offer techniques to ensure adequate nutri­tion and hydration

  Describe the plan for posttreatment follow-up, including knowledge of recurrent symptoms

  Modify the prescribed regimen as directed by a health care professional


Your client is prescribed IV ciprofloxacin (Cipro) for pyelonephritis. She is also prescribed 25 mg meperidine every 3 hours prnfor her pain. Radiographic studies are deferred at this time because of her pregnancy. A urine culture indicates that the infecting organism is £ coli, and the sensitivity of the bacteria to ciprofloxacin is confirmed. After 3 days her pain is absent, her fever is resolved, and her urinary symptoms are clearing. She is to be discharged today and is to continue tak­ing her antibiotic orally at home. A follow-up medical visit is scheduled in 7 days.

 What discharge planning and health care teaching are indi­cated at this time?

Renal Abscess


An abscess is a collection of fluid and cells caused by an in­flammatory response to bacteria. An abscess may occur within the renal parenchyma (renal abscess), in the renal and Gerota's fascia (perinephric abscess), or in the flank. An ab­scess is suspected when fever and symptoms are not relieved promptly by antibiotic therapy.


A renal or perirenal abscess is readily diagnosed via sonogra-phy or a computed tomography (CT) scan. Arteriography andradionuclide scintillation methods (e.g., gallium scan) also may be useful for diagnosis. Symptoms of renal abscess in­clude fever, flank pain, and general malaise. Local fl edema and erythema may be observed.

Drainage by surgical incision or needle aspiration is often necessary. Appropriate broad-spectrum antibiotics are "also prescribed.

Renal Tuberculosis


The genitourinary tract is the most common extrapulmonary site of tuberculosis. Approximately 10% of new cases of tu­berculosis are extrapulmonary (Tolkoff-Rubin, Cotran, & Rubin, 2000). Tuberculosis of the kidney is sometimes called granulomatousnephritis. After Mycobacterium tuberculosis invades the kidneys, usually by a bloodborne route, an in­flammatory response is activated and forms scar tissue (granuloma) that replaces normal kidney tissue.


Clients may experience urinary frequency, dysuria, hematuria and/or proteinuria, flank pain or renal colic secondary to the passage of clots or stones, pyuria, and hypertension. Skin test (e.g., purified protein derivative [PPD]) or chest x-ray film ev­idence of tuberculosis may or may not be present.

Clients with current or previous pulmonary tuberculosis who show signs of unexplained fever, hematuria, and sterile pyuria are at high risk for renal tuberculosis. The diagnosis is made through a urine culture of three clean-catch, first-morning specimens. Other genitourinary sites for tuberculosis include the prostate, epididymis, ureters, testes, bladder, and seminal vesicles.

Antitubercular therapy is the primary treatment. Recom­mendations include a 2-month course of rifampin, isoniazid, andpyrazinamide followed by 4 months of rifampin and isoni­azid. Three to six more months of rifampin and isoniazid may be recommended for men who may be harboring the organism in the prostate (Tolkoff-Rubin, Cotran, & Rubin, 2000).

Complications include the loss of renal function, nephro-lithiasis, obstructive uropathy, and bacterial superinfection of the urinary tract. Surgical excision of diseased tissue may be indicated to preserve renal function.




Renal disorders interfere with the ability of the kidney to filter wastes and to balance fluid and solutes. The kidneys work in an integrated way with so many other organ systems; therefore a renal disorder can significantly affect systemic health and lead to life-threatening outcomes. Renal disorders can be categorized as congenital, obstructive, infectious, glomerular, and degenerative. Renal tumors and renal trauma are also described in this chapter.

Polycystic Kidney Disease


Polycystic kidney disease (PKD) is one of the most common inherited disorders and affects 250,000 to 500,000 people in theUnited States. It can be inherited as either an autosomal dominant trait or, less commonly, as an autosomal recessive trait. People who inherit the recessive form of PKD usually die in early childhood. The 5% to 10% incidence of PKD in clients with no family history occurs as a result of a sponta­neous genetic mutation. PKD is more common in Caucasians than in people of other races.



Fluid-filled cysts in the epithelial cells of the nephron charac­terize PKD. In the dominant form only 5% to 10% of nephronsmay be involved until the fourth decade of life, whereas in the autosomal recessive form nearly 100% of nephrons are in­volved at birth. Cysts develop as a result of kidney cell prolif­eration, altered secretion, and abnormal cell matrix biology (Avner, et al., 1999; Calvet& Grantham, 2001).

Cysts can develop anywhere in the nephron. Over time, small cysts become progressively larger (up to a few centime­ters in diameter) and more widely distributed; the glomerular and tubular membranes are damaged. As the cysts become filled with fluid, thenephron functions of filtration, reabsorp-tion, and secretion become less effective.

The kidney tissue is eventually replaced by nonfunctioning cysts, which look like a cluster of grapes (Figure). The kidneys are grossly enlarged; each cystic kidney may enlarge to two or three times its normal size, becoming as large as a football. Other abdominal organs are displaced, and the client has considerable discomfort. The fluid-filled cysts are also prone to infection, rapture, and bleeding.

More than 60% of clients with PKD have high blood pres­sure. The cause of hypertension in this disorder is thought to be related to renal ischemia from the enlarging cysts. As the ves­sels are compressed and renal blood flow decreases, the renin-angiotensinsystem is activated, raising blood pressure. Control of hypertension is a top priority because proper treatment can interrupt the vasoconstriction that leads to renal ischemia.

Cysts may also occur in other tissues, such as the liver, blood vessels of the brain, and cardiac blood vessels. Cysts may alter liver function or result in spontaneous rapture of vascular cysts (berry aneurysms) in the brain, causing sudden death. For reasons as yet unknown, kidney stones occur in 8% to 36% of the clients with PKD. Heart valve abnormalities (e.g., mitral valve prolapse), left ventricular hypertrophy, and colonic diverticuli also are more prevalent in clients with PKD.


PKD has at least two inherited forms. Men and women have an equal chance of inheriting the disease because the gene re­sponsible for PKD is not located on the sex chromosomes. The offspring of parents who have PKD have a 50% proba­bility of inheriting the gene that causes the autosomal domi­nant form of the disease.

Manifestations of autosomal dominant polycystic kidney disease (ADPKD) usually do not appear until the fourth decade of life. Half of the affected people develop renal fail­ure by age 50 years. ADPKD-1 is the most severe form both in disease progression and in mortality. ADPKD-2 involves a slower rate of cystic formation and growth, resulting in a de­layed progression to renal failure and other complications.

At present, there is no way to prevent PKD, although early detection and management of hypertension may slow the pro­gression of renal impairment. Genetic counseling and evalua­tion may be useful for adults who have one parent or both parents with PKD. For those whose clinical symptoms do not appear until after the childbearing years, offspring can be in­cluded in genetic counseling sessions.




The nurse explores the family history of a client with sus­pected or actual PKD and asks whether either parent was known to have PKD or whether there is any family history of kidney disease. The age at which signs and symptoms devel­oped in the parent and any related complications may have prognostic significance. The client is asked about constipa­tion, abdominal discomfort, a change in urine color or frequency, high blood pressure, headaches, and a family history of sudden death from a stroke.


Chart 71-1 lists key features of PKD. Pain is the presenting symptom in 20% to 30% of clients and islioted in at least 60%. The nurse inspects the abdomen. A protruding and distended abdomen is common as the cystic kidneys swell and push the abdominal contents forward. Polycystic kidneys are easily pal­pated because of their increased size. The nurse proceeds with gentle abdominal palpation because the cystic kidneys and nearby tissues may be tender, and palpation is uncomfortable.

The client also may have flank pain as a dull ache or as sharp and intermittent discomfort. Dull and aching pain is caused by increased kidney size with distention or from in­fection within the cyst. Sharp, intermittent pain occurs in re­sponse to a ruptured cyst or the presence of a stone. When a cyst ruptures, the client may notice bright red or cola-colored urine. The nurse suspects infection if the urine is cloudy or foul smelling or if there is dysuria (pain on urination).

Nocturia (the need to urinate excessively at night) may be an early disease sign and occurs because of decreased renal concentrating ability. As renal function further declines, the client experiences increasing hypertension, edema, and ure-micsymptoms such as anorexia, nausea, vomiting, pruritus, and fatigue. Because berry aneurysms often occur in clients with PKD, a severe headache with or without neurologic or vision alterations deserves particular attention.


As an inherited disorder, PKD may cause complex psychoso-cial responses. The client often has had direct experience with the effects and consequences of the disease in other close family members. He or she may have had a parent who died or other close relatives who required dialysis or transplanta­tion. While obtaining the family history, the nurse listens carefully for spoken and unspoken feelings of anger, resent­ment, hostility, futility, sadness, or anxiety; such feelings may need further exploration. The focus may be one or both par­ents or the process of diagnosis and treatment. Feelings of guilt and concern for the client's own children may further complicate the adjustment.


Urinalysis usually reveals proteinuria (protein in the urine) once the glomerali are involved. Hematuria may be gross ormicroscopic. Bacteria in the urine suggest an infection, usu­ally in the cysts. A urine sample for culture and sensitivity testing is obtained when there is clinical or laboratory evi­dence of infection. As kidney function deteriorates, serum creatinine and blood urea nitrogen (BUN) levels rise. With worsening kidney function, the 24-hour creatinine clearance decreases. Renal handling of sodium may cause either sodium losses or sodium retention.

Diagnostic studies include renal sonography, computed to­mography (CT), and magnetic resonance imaging (MRI).

Small cysts are detectable by sonography, CT, or MRI. Renal sonography provides diagnostic evidence of PKD, with mini­mal risk in most cases.


Common nursing diagnoses for the client with polycystic kid­ney disease (PKD) include Acute Pain, Chronic Pain, and Constipation. Common collaborative problems include Po­tential for Infection, Hypertension, Stone Formation, or Renal Failure. Chart 71-2 lists some NIC interventions for clients with renal disorders. (See Chapter 70 for information on renal infections and stone formation. See Chapter 72 for care of the client with renal failure.)



Comfort strategies include pharmacologic, physical, and inte-grative approaches. A combination may be most effective. Non-steroidal anti-inflammatory agents (NSAIDs) are used cau­tiously because of their tendency to adversely affect renal function. Aspirin-containing compounds are avoided to prevent an increased potential for bleeding.

If cyst infection is the cause of discomfort, the physician orders a lipid-soluble antibiotic such as trimethoprim/ sulfamethoxazole(Bactrim, Septra, Trimpex) or ciprofloxacin (Cipro), which penetrate the cyst wall. Monitoring serum cre-atinine levels is necessary because antibiotic therapy can be nephrotoxic. Applying dry heat to the abdomen or flank may promote comfort when renal cysts are infected. When pain is severe or debilitating, cysts can be decompressed with percu­taneous needle aspiration and drainage.

The nurse teaches the client methods of enhancing relax­ation and promoting comfort via deep breathing, guided im­agery, or other relaxation strategies. The overall goal is client self-management.


 BOWEL MANAGEMENT. The nurse also teaches the client how to prevent constipation. The teaching plan covers adequate fluid intake, the role of increased dietary fiber when fluid intake is more than 2500 mL/24 hr, and the need for reg­ular exercise to achieve regular bowel elimination. The nurse explains that pressure on the large intestine may further im­pede peristalsis as the polycystic kidneys increase in size. Consequently, the client should know that these recommen­dations for bowel management might change, particularly if renal failure also develops. The nurse also advises about the appropriate use of stool softeners and bulk agents, including the careful use of laxatives, to prevent complications related to chronic constipation.


 TEACHING: DISEASE PROCESS; TEACHING: PRE­SCRIBED MEDICATION. Blood pressure control is neces­sary to minimize cardiovascular complications and slow the progression of renal dysfunction. Nursing interventions in­clude education to promote self-management and understand­ing (see Chapter 36 for more information on hypertension). When renal impairment is evident through a decreased con­centrating ability (e.g., nocturia, low urine specific gravity), the nurse encourages the client to drink at least 2 L of fluid per day to prevent fluid volume deficit, which could further affect renal function. Restricting excess dietary sodium intake may control blood pressure. Because fluid volume intake is not restricted, intravascular volume depletion and decreased renal perfusion does not occur.

Medications for blood pressure control include antihyper-tensive agents and diuretics. Antihypertensive agents include angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, beta blockers, and vasodilators (see Chart 36-2). ACE  inhibitors show promise in controlling  the epithelial-proliferative aspects of PKD and in reducing mi-croalbuminuria (Torra, 1999). If PKD progresses to chronic renal failure or end-stage renal disease, treatment approaches are similar to those in Chapter 72.

The nurse teaches the client, family, or significant other how to measure and record blood pressure. The nurse also helps the client establish a schedule for self-administering medications, monitoring daily weights, and keeping blood pressure records (Chart 71-3). The potential side effects of the medications are explained. The nurse makes written ma­terials, such as medication teaching cards and booklets, available.

A low-sodium diet is often prescribed to control the hy­pertension that usually accompanies PKD. However, some clients may experience salt wasting and do not require a sodium-restricted diet. As the disease progresses, the physician may limit the client's protein intake to slow the development of renal failure. The nurse assists the client, family, or significant other in understanding the recom­mended diet plan and clarifies its rationale. The nurse works closely with the dietitian to foster the client's under­standing. The nurse may also initiate a referral for nutri­tional counseling.

Health Care Resources

The Polycystic Kidney Research Foundation conducts re­search and provides education about PKD. Many publications are available on request; there is a fee for some materials. Chapters of the National Kidney Foundation (NKF) and the American Association of Kidney Patients (AAKP) may also provide resources for client information and support.


Hydronephrosis, Hydroureter, and Urethral Stricture


Hydronephrosis and hydroureter are disorders usually associ­ated with the obstruction of urine outflow. Urethral strictures also obstruct outflow. Prompt recognition and treatment are crucial to prevent permanent renal damage.

In hydronephrosis, the kidney becomes enlarged as urine accumulates in the pelvis and kidney tissue. Because the capacity of the renal pelvis is normally 5 to 8 mL, obstructions within it or at the ureteropelvic junction (UPJ) quickly result in renal pelvic distention. Kidney medullary pressure in­creases as the volume of urine increases. Over time, some­times in only a matter of hours, the blood vessels and renal tubules can be damaged extensively.

 In clients with hydroureter, the pathophysiologic effects are similar but the obstruction is lower in the urinary tract. The ureter is most likely to become obstructed where the iliac vessels cross or at the ureterovesical entry. Dilation of the ureter above the point of obstruction results in enlargement as urine continues to accumulate.

In a client with a urethral stricture, the obstruction is very low in the urinary tract; this causes bladder distention to occur beforehydroureter and hydronephrosis. The problems and kidney damage are similar without prompt treatment.

A urinary obstruction can cause structural damage when pressure builds up directly on tissue. Tubular filtrate pressure also increases within the nephron as drainage through the col­lecting system is impaired. With this added pressure, glomeru-lar filtration decreases or ceases, and renal failure results. Ni­trogenous waste products (urea, creatinine, and uric acid) and electrolytes (sodium, potassium, chloride, and phosphorus) are retained in the serum, and renal regulation of acid-base bal­ance is impaired.

Disorders that can cause hydronephrosis or hydroureter in­clude tumors, stones, trauma, congenital structural defects, and retroperitoneal fibrosis. Early treatment of the causes can prevent hydronephrosis and hydroureter and thus prevent per­manent renal damage. The specific time needed to prevent per­manent damage varies and depends on the client's underlying renal status. Permanent damage may occur in less than 48 hours in some clients and after several weeks in other clients.



The nurse obtains a history from the client, focusing on known renal or urologic disorders. A history of childhood uri­nary tract problems may signal the presence of previously unidentified structural defects. The nurse inquires about the client's pattern of urination, especially its amount, frequency, color, clarity, and odor. The client is asked about recent flank or abdominal pain. Chills, fever, and malaise may be present with a urinary tract infection (UTI).

The nurse inspects each flank to identify asymmetry, which may occur with a renal mass, and gently palpates the client's abdomen to identify any areas of tenderness. The uri­nary bladder is also palpated and percussed to detect disten­tion. Gentle pressure on the abdomen may cause urine leak­age, which reflects a full urinary bladder and possible obstruction of the bladder/urethral junction.

Urinalysis may show bacteria or white blood cells if infec­tion is present. When urinary tract obstruction is prolonged, mi­croscopic examination may reveal tubular epithelial cells. The chemical analysis of serum is normal unless decreased glomerularfiltration has occurred; serum creatinine and blood urea nitrogen (BUN) levels increase with a decreased glomeru­lar filtration rate (GFR). Serum electrolyte levels may also be altered and indicate hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis (bicarbonate deficit).

Intravenous urography reveals ureteral or renal pelvis dila­tion. Urinary outflow obstruction may be revealed by sonog-raphy (renalechography) or computed tomography (CT).


 FLUID MONITORING; URINARY RETENTION CARE; INFECTION PROTECTION. Urinary retention and potentialfor infection are the primary problems. Failure to treat the cause of urinary obstruction may lead to infection and renal failure. Surgery is usually required to remove or reduce the cause of the obstruction.


DEGENERATIVE DISORDERS                                             

Degenerative disorders that cause changes in renal function are usually associated with the damage or effects caused by amultisystem disorder. Many of these degenerative disorders result from changes in kidney blood vessels.



Nephrosclerosis is a problem of changes in the nephron blood vessels. Vessel walls thicken, and the vessel lumen nar­rows. As a result, renal blood flow is decreased and kidney tis­sue is chronically hypoxic. Ischemia and fibrosis develop over time.

Nephrosclerosis is associated with all types of hyperten­sion, atherosclerosis, and a history of diabetes mellitus. The more severe the hypertension, the greater the risk for exten­sive kidney damage. Nephrosclerosis is rarely seen when blood pressure is consistently below 160/110 mm Hg. The changes associated with hypertension may be reversible or within may progress to end-stage renal disease (ESRD) months or years.

Hypertension is the second leading cause of ESRD. Ap­proximately 30% of clients requiring lifesaving renal replace­ment therapy (e.g., dialysis or transplantation) have hyperten­sion as the cause of their renal failure (NIDDK).


 Hypertension is more common in African Americans, and the risks of ESRD from hypertension are also greater for African Americans (Bakris et al., 2000). Between the ages of 25 and 45 years, the ratio of African Americans to Caucasians at risk for ESRD from hypertension is nearly 20:1 (Richardson & Piepho, 2000). These findings do not suggest that ESRD fromnephrosclerosis does not occur in Caucasians but rather that affected Caucasians are likely to be older.


 Treatment aims to control high blood pressure and preserve renal function. Although many antihypertensive drags may lower blood pressure, the client's response is important in en­suring long-term adherence to the prescribed therapy. Factors promoting adherence include regimen simplicity (e.g., once-a-day dosing), low cost, and minimal side effects. Lack of basic knowledge or misinformation about hyper­tension poses additional challenges to nurses and all health care providers working with hypertensive clients. When evi­dence of renal disease occurs, adherence to therapy is even more important for preserving health.

Many medications can control high blood pressure (see Chart 36-2); more than one agent may be necessary. Angiotensin-converting enzyme (ACE) inhibitors are particu­larly useful in reducing hypertension and preserving renal function. Diuretics can maintain fluid and electrolyte balance in the presence of renal insufficiency. Caution is required to prevent hyperkalemia when potassium-sparing diuretics (e.g., triamterene or spironolactone) or combination agents contain­ing a potassium-sparing diuretic are used for clients with known renal disease.

Renovascular Disease


Pathologic processes affecting the renal arteries may result in severe lumen narrowing and drastically reduced blood flow to the renal parenchyma. Uncorrected renovascular disease, such as renal artery stenosis or thrombosis, causes ischemia and atrophy of renal tissue.

Renovascular disease is suspected with a sudden onset of hypertension, particularly in clients older than 50 years. Clients with high blood pressure but with a negative family history for hypertension may also be considered potential candidates for renal arterystenosis (RAS).

RAS from atherosclerosis or fibromuscular hyperplasia (in­creased amount of tissue) is the primary cause of renovascular disease. Other causes include thrombosis and renal aneurysms.

Atherosclerotic changes in the renal artery are often asso­ciated with sclerosis in the aorta and other major vessels. Changes in the renal artery are close to where the renal artery and aorta meet. Fibrotic changes of the vessel wall occur throughout the length of the renal artery.



Key features of renovascular disease are listed in Chart 71-8. The onset of hypertension is usually after age 40 to 50 years, and the family history is often negative for hypertension. Di­agnosis is made by renal arteriography; measurement of renal vein renin levels provides additional evidence but may not be confirmatory. A renal arteriogram visualizes the renal vascu-lature and offers critical information for invasive treatment. The comparison of renal vein renin levels may reveal which kidney is producing more renin.


Visualization of the type of defect, extent of narrowing, and surrounding vasculature is critical to decide treatment inter­vention. The client's overall condition and the size of the at­rophied kidney further influence decisions about intervention. RAS may be treated by drugs to control high blood pres­sure and by percutaneous transluminal balloon angioplasty or by surgical bypass procedures to restore the renal blood sup­ply. Drugs may control high blood pressure but may not lead to long-term preservation of kidney function. In young and middle-aged adults, a lifetime of treatment with multiple agents for high blood pressure may make treatment difficult and the outcomes uncertain.

KEY FEATURES of Renovascular Disease

·       Significant, difficult to control btood pressure

·           Elevated serum creatinine

·       Decreased creatinine clearance

Balloon angioplasty is considered less risky and requires much less time for recovery than does renal artery bypass sur­gery (see Chapter 36). Renal artery bypass surgery is a major procedure and involves at least 2 months for convalescence. A bypass may be performed for either one or both renal arteries. The surgeon inserts a synthetic graft that redirects blood flow from the abdominal aorta into the renal artery, beyond the area of stenosis. Increasingly, splenorenal bypass procedures can also restore renal blood flow. Technically, the process is similar to other arterial bypass procedures (see Chapter 36).

For clients with RAS, the diagnostic and treatment alter­natives present tremendous decisional conflict. Clients often experience a deterioration of renal function, as noted by ele­vated serum creatinine levels and decreased creatinine clear­ance. These clients are at increased risk for acute renal failure from the administration of nephrotoxic agents such as ra-diopaque contrast media and from possible intraoperative hy-potensive episodes. However, no treatment probably means that dialysis is inevitable.

Diabetic Nephropathy


Diabetes mellitus is the leading cause of end-stage renal dis­ease (ESRD) among Caucasians in the United States. Ap­proximately 36% of clients requiring dialysis or renal trans­plantation have diabetes mellitus as the primary contributing factor (NIDDK). The cost of preventing or reducing re­nal problems among clients with diabetes is offset by the high cost of treating severe renal diseas. Diabetic nephropathy may result from type 1 or type 2 diabetes mellitus. Diabetic renal disease is influenced by the extent, duration, and effects of atherosclerosis, hyper­tension, and autonomic neuropathy, which promotes bladder atony, urinary stasis, and urinary tract infection.

Immunologic response mechanisms have also been impli­cated in glomerular basement membrane thickening and other changes in clients with diabetic renal disease. Investigations continue to explore if defects are the result of genetic or meta­bolic disturbances.


Diabetic nephropathy is a microvascular complication of dia­betes defined by persistent albuminuria (as shown by dipstick or a urinary albumin excretion rate above 0.3 g/dL), without evidence of other renal disease. A diagnosis of renal disease in clients with diabetes mellitus is made on the basis of the history and clinical examination. Diabetic renal disease is progressive (Table 71-4).Structural and functional changes occur in the kidneys of diabetic clients. Initially, kidney size is slightly increased and glomerularfiltration rates (GFR) are higher than normal. A radioimmunoassay of urine detects the microlevels of albu­min associated withalbuminuria. Progressive renal damage occurs before dipstick procedures can detect protein in the urine. For most clients, proteinuria(albuminuria) indicates the need for a renal biopsy for further diagnosis. For the client with diabetes, observed microvascular changes in the retinacorrelate well with the renal microvascular changes. Exami­nation of the retina showing capillary leakage, fibrosis, and the typical changes of diabetic retinopathy eliminates the need for a risky renal biopsy.

As with nephrotic syndrome, proteinuria may be mild, mod­erate, or severe. Clients with diabetes mellitus are always con­sidered to be at risk for renal failure. If possible, nephrotoxic agents (e.g., radiopaque contrast media or aminoglycosides) and fluid volume deficit are avoided. Clients with worsening renal function may begin to have frequent hypoglycemic episodes and a decreased need for insulin or oral antihyperglycemic agents. The nurse explains to the client that the kidneys metabolize and excrete insulin. When renal function deteriorates, the insulin is available for a longer time and thus less of it is needed. Unfor­tunately, many clients believe this means their diabetes mellitus is improving. The result is accelerated progression to ESRD. (See Chapter 65 for more information on diabetic nephropathy.)

Care of the client with chronic renal insufficiency is thought to be more effective when a multidisciplinary case managementapproach is used. Research has not demonstrated a clear ad­vantage to such an approach (see the Evidence-Based Practice forNursing box above).


Cysts and Benign Tumors


Benign urinary tract growths include cysts and tumors of the renal parenchyma or urinary bladder. Because malignant growths may occur within cystic structures, a thorough eval­uation is essential. A simple renal cyst grows out of renal parenchymal tissue, usually the cortical tissue. The cyst is filled with fluid and can cause local tissue destruction as it enlarges. Many cysts cause no symptoms and are discovered accidentally during fluoro-scopic examination or autopsy.

Although the exact cause is unknown, cysts are usually considered a structural defect that occurs prenatally. The eti­ology and incidence of benign tumors is also unknown. Thus far there are no recognized methods of prevention.


Diagnosis of a simple renal cyst involves IV urography, sonography, and computed tomography (CT). If the cyst ap­pears to be filled with fluid at urographic examination, a sonography is generally recommended; if the cyst appears denser, a CT scan is needed.

Treatment may consist of percutaneous aspiration of a fluid-filled cyst or surgical exploration with the potential for total or subtotalnephrectomy.

Renal Cell Carcinoma


Renal cell carcinoma is also referred to as adenocarcinoma of the kidney. As with other malignancies, the healthy tissue of the kidney is replaced and displaced by cancer cells. Although the exact mechanism is not known, the tumor cells are thought to originate in the proximal convoluted tubules of the nephron.

Systemic effects occurring with the cancer are called paraneoplastic syndromes and include anemia, erythrocy-tosis,hypercalcemia, liver dysfunction with elevated liver en­zymes, hormonal effects, increased sedimentation rate, and hypertension.

Anemia and erythrocytosis may appear contradictory: There is some blood loss from hematuria, but the amount lost is not sufficient to cause anemia. Erythrocytosis may be caused by erythropoietin production in the tumor cells. Hy­pertension may result from increased renin.

Parathyroid hormone produced by tumor cells may be the cause of hypercalcemia; other hormone alterations include in­creasedrenin levels (causing hypertension) and increased hu­man chorionic gonadotropin (hCG) levels, which are accom­panied by decreased libido and changes in secondary sex characteristics. The cause of the increased sedimentation rate and changes in liver function studies is not known.

Renal tumors are categorized into four stages (Table 71-5). Complications include metastasis and urinary tract obstruc­tion. Metastasis usually occurs via the blood or lymph to the adrenal gland, liver, lungs, long bones, or the other kidney. When the tumor surrounds a ureter, hydroureter and urinary tract obstruction may result.

The exact cause of renal cell carcinoma is unknown, but links to tobacco use and exposure to chemicals such as lead, phosphate, and cadmium have been observed. Other studies suggest the possibility of hereditary influences.

Renal malignancies account for approximately 2% of re­ported cancers, with about 28,800 new cases and 11,300 deaths annually in the United States. The 5-year survival rate is 60% in the United States (Bonsib, 1999). Renal cell carci­noma usually affects clients between 55 and 60 years of age.





The nurse asks the client for specific information, including age, known risk factors (e.g., smoking or environmental ex­posures), history of weight loss, changes in urine color, ab­dominal or flank discomfort, and fever. The cause of fever is unknown, butpyrogens produced by the tumor cells have been implicated.


Presentations of renal carcinoma are seen only in 5% to 10% of clients and include flank pain, gross hematuria, and a pal­pable renal mass. The nurse asks about the nature of the flank or abdominal discomfort; clients typically describe the pain as dull and aching. The pain may be more intense if bleeding into the tumor occurs. The nurse inspects the flank, noting asymmetry or obvious protrusions. An abdominal mass may be detected through gentle palpation. A renal bruit may be heard on auscultation.

Hematuria is a late common sign. Blood in the urine may be grossly observable as bright red flecks or clots, or the urine may appear smoky or cola colored. Without gross hematuria, microscopic examination may or may not reveal red cells.

The skin is inspected for pallor, darkening of the nipples and breast enlargement (in men). Other findings may include muscle wasting, weakness, generally poor nutritional status, and weight loss. All tend to occur late in the disease.


Urinalysis may reveal red blood cells. Hematologic studies re­veal decreased hemoglobin and hematocrit values, hypercal­cemia, increased erythrocyte sedimentation rate, and increased levels of adrenocorticotropic hormone, human chorionic go­nadotropin(hCG), cortisol, renin, and parathyroid hormone.

Renal masses may be detected by surgical exploration, IV urogram with nephrograms, or sonography. The mass and sur­rounding structures may be further delineated by CT with contrast or magnetic resonance imaging (MRI). Staging or determining the extent of tumor spread is best accomplished with renal arteriography and renal venography.


Interventions focus on controlling the cancer and preventing metastasis.

NONSURGICAL MANAGEMENT. Chemotherapy with a variety of agents has had limited effectiveness. The Food and Drug Administration (FDA) has approved expanded clinical trials for the study of interleukin-2 (IL-2), a biologic response modifier (see Chapters 20 and 25). Interferon (INF) and tu­mor necrosis factor (TNF) are also being used investigation-ally. Studies withlymphokine-activated killer (LAK) cells and tumor-infiltrating lymphocytes (TIL) are in the clinical trial stage.

SURGICAL MANAGEMENT. Renal cell carcinoma is usually treated surgically by nephrectomy (kidney removal) when pain, bleeding, or tumor spread cannot be controlled otherwise.

PREOPERATIVE CARE. The client is instructed about surgical routines (see Chapters 17, 18, and 19). The nurse ex­plains the probable site of incision and the postoperative dress­ings, drains, or other equipment needed and reassures the client about pain relief. Preoperative care includes administer­ing blood and fluids to achieve hemodynamic stabilization.

OPERATIVE PROCEDURE. The client is placed in the lateral position with the operative kidney uppermost; after po­sitioning the arms and legs, the client's trunk area is flexed to increase exposure of the kidney area. Removal of the eleventh or twelfth rib is needed to provide better access to the kidney. The surgeon removes the entire kidney, renal artery and vein, and surroundingGerota's fascia after ligation of the ureter. The adrenal gland is left intact. A drain may be placed in the wound before closure.

When a radical nephrectomy is performed, the periaortic lymph nodes are also removed, the surgical approach may betransthoracic (as discussed in the previous paragraph), lum­bar, or transabdominal depending on the size and location of the lesion.Radiation therapy may follow a radical nephrec­tomy. Studies are ongoing to identify the effectiveness of ad­juvant therapy (e.g., chemotherapy).

POSTOPERATIVE CARE. Refer to Chapter 19 for post­operative care. Assessment of urologic and renal function is essential to determine function in the remaining kidney.

Monitoring. The nurse observes the client's abdomen for distention from bleeding and symptoms of adrenal insuffi­ciency. The nurse observes the bed linens under the supine client, because bleeding may be present. Hemorrhage or adre­nal insufficiency may be accompanied by hypotension, a de­crease in urine output, and an altered level of consciousness.

A decrease in blood pressure is one of the earliest signs of both hemorrhage and adrenal insufficiency; in clients with hy­potension, urine output also decreases immediately. Large water and sodium losses in the urine occur in clients with ad­renal insufficiency; consequently, a large urine output is fol­lowed by hypotension and subsequent oliguria (<400 mL/24 hr or less than 25 mL/hr). The physician may prescribe IV re­placement of fluids and the administration of packed red blood cells.

The second kidney is expected to provide adequate renal function. The nurse assesses urine output hourly for the first 24 hours postoperatively; a urine flow of 30 to 50 mL/hr is ac­ceptable. Flow rates of less than 25 to 30 mL/hr suggest a de­crease in renal perfusion. Initially, the postoperative hemoglobin level, hematocrit values, and white blood cell count may be measured every 6 to 12 hours.

The nurse monitors the client's temperature, pulse rate, and respiratory rate at least every 4 hours; careful measure­ment and recording of fluid intake and output are critical. The client is weighed daily.

The client may be in a special care unit for 24 to 48 hours postoperatively for monitoring of bleeding and/or adrenal in­sufficiency. A drain placed near the site of incision removes residual fluid. Because of the discomfort associated with lung expansion, the client is susceptible to atelectasis. Fever, chills, thick sputum, or decreased breath sounds suggest pneumonia.

Pain Management. After surgery, opioid analgesics (e.g., meperidine [Demerol], hydromorphone [Dilaudid], and mor­phine sulfate [Statex*^]) are given parenterally. The incision site, in which the major muscle groups associated with breath­ing and movement are involved, necessitates the liberal use of analgesic agents. These medications may be required for 3 to 5 days for pain management. Oral analgesic agents may be con­sidered when the client is permitted to eat and drink.

Prevention of Complications. One or more antibiotics may be prescribed for intraoperative and postoperative pro­phylaxis. These agents are usually given as single-dose pre­scriptions. The need for additional antibiotics is based on clin­ical and laboratory evidence of infection. Steroid replacements may be necessary in adrenal insufficiency.



Trauma to one or both kidneys is always a concern in pene­trating wounds or blunt injuries to the back, flank, or ab­domen. Injury to the kidney can be minor, major, or pedicle. Strategies to prevent trauma are reviewed in Chart.

Minor injuries include contusions, small lacerations, and disruption of the integrity of the parenchyma and the calyx (forniceal disruption). In a person with a contusion, one or both kidneys sustained a bruise because of the major impact. Small blood vessels may be damaged, causing some hematuria. One or more small lacerations may result in small, lo­calized hematomas. There may also be a small hematoma at the site of forniceal disruption. Common causes include falls, contact sports, and blows to the back and torso.

Major injuries involve lacerations to the cortex, medulla, or one of the segmental branches of the renal artery or vein. Deepparenchymal injuries may extend throughout the kidney and result in hematomas contained within or disrupting the capsule. Otherparenchymal injuries involve the cortex and cause shattering of tissue, resulting in either an intact or a dis­rupted capsule.

A major injury is most likely to follow a penetrating ab­dominal, flank, or back wound (such as seen with gunshot wounds, knife wounds, or motor vehicle accidents). Bleeding is extensive, and surgical exploration is often required. Because of the hemorrhage,hypoperfusion of renal parenchyma can produce short-term or long-term renin-induced hypertension

Pedicle injuries involve a laceration or disruption of the re­nal artery and/or renal vein. Hemorrhage is extensive and rapid, and death may ensue quickly unless diagnosis and in­tervention are prompt.



The nurse obtains a history of the client's usual health status and the events surrounding the trauma from the client, a wit­ness, or emergency personnel. Critical assessment information includes a history of renal or urologic disease, surgical intervention, or systemic health problems (e.g., diabetes mel-litus or hypertension).

Ureteral and/or renal pelvic injury may cause diffuse ab­dominal pain, local collections of urine, and infection. The nurse asks the client about pain, specifically flank or abdom­inal pain, and solicits a description: Is the pain dull? Sharp? Constant? Intermittent?Aggravated by coughing?

The nurse measures the client's blood pressure and apical and peripheral pulse rates, respiratory rate, and temperature. The right and left flanks are inspected to determine asymmetry or penetrating injuries of the lower thorax or back. Similarly, the nurse inspects the abdomen for ecchymoses, percusses the abdomen for distention, and observes for penetrating wounds. The urethra is inspected for gross bleeding.

Urinalysis commonly reveals hemoglobin or red blood cells from the rupture of small or large renal blood vessels. Microscopic examination of the urine may also show red blood cell casts, which suggest tubular damage. Hemoglobin and hematocrit values decrease with blood loss; the white blood cell count is elevated with inflammation or infection.

Fluoroscopic procedures include IV urography, renal arte-riography, and computed tomography (CT). A urogram re­veals the number of kidneys and the integrity and patency of the collecting system. Renal sonography is an alternative di­agnostic procedure to a urogram that avoids radiopaque con­trast media exposure to clients with elevated serum creatinine levels.

Renal arteriography reveals the number of kidneys and, more specifically, the blood supply to each. In clients with pedicle injuries, the contrast media used in arteriography extravasates from the ruptured vessels, and the renal parenchyma is not visualized. The CT scan shows the location of the injury and vascular and tissue integrity. Intracapsular and extracapsular hematomas are readily observable on the CT scan.


Nursing diagnoses for the client with renal trauma include In­effective (Renal) Tissue Perfusion, Anxiety, Pain, Impaired Uri­nary Elimination, Post-Trauma Syndrome, and Risk for Infec­tion. Interventions include medications for vascular support, fluids to restore fluid volume, and surgery when indicated.


DRUG THERAPY. Prescribed IV dopamine (Revimine4*1, others) supports renal perfusion. Coagulation factors such as vitaminÊ and platelets are assessed and administered as needed.

FLUID THERAPY. Fluid administration to restore circu­lating blood volume is critical for renal tissue perfusion. Crys­talloidsolutions replace water and some electrolytes and in­clude 0.9% sodium chloride (NSS), 5% dextrose in 0.45% sodium chloride, and Ringer's solution. When significant bleeding has occurred, whole blood or packed red cell re­placement restores the oxygen-carrying capacity of hemoglo­bin. Plasma volume expanders, such as dextran or albumin, help re-establish plasma oncotic pressure and minimize fluid shift from the intravascular to the interstitial fluid space.

During fluid resuscitation or restoration, the nurse admin­isters fluid at the prescribed rate and monitors the client for hemodynamicinstability. The nurse also monitors vital signs as often as every 5 to 15 minutes and measures and records urine output hourly. Urine output should be greater than 25 to 30 mL/hr.

SURGICAL MANAGEMENT. Surgical interventions may include nephrectomy and partial nephrectomy. For clients with major vascular tearing, the kidney may be surgically re­moved, repaired through revascularization techniques, and then reimplanted. The repair of kidney tissue outside the client is called bench surgery. Autotransplantation is trans­plantation of one's own kidney.

Community-Based Care

The nurse instructs the client, family, or significant other about the effects of the injury and how to assess for infection or other complications, such as the onset of bleeding or uri­nary retention. The client is instructed to observe the pattern and frequency of urination and to note whether the color, clar­ity, and amount appear normal. The nurse also instructs the client to seek medical attention if these characteristics change significantly and if a feeling of bladder distention or inade­quate bladder emptying occurs, which suggests an obstruc­tion. Chills, fever, lethargy, and/or cloudy, foul-smelling urine may suggest a urinary tract infection. The nurse warns the client not to ignore these symptoms and to seek medical care promptly if they occur.



Acute and chronic renal failure have become increasingly niore common in the United States, resulting in considerable morbidity and mortality. Acute renal failure is responsible for 7% of all hospital admissions, and the prevalence of end-stage renal disease has virtually doubled in the last decade (Stark, 1998; U.S. Renal Data Systems, 1999). There are many causes of renal failure, but complications related to poorly controlled diabetes remain the most common cause.

The functions of the kidney are excretion of waste, water and salt regulation, maintenance of acid balance, and hor­mone secretion. When renal function deteriorates gradually, as occurs with most causes of chronic renal failure, 90% to 95% of the nephrons must be destroyed before significant re­nal failure is evident. The client may have many years of de­creased renal reserve and chronic renal insufficiency before the uremia of end-stage renal failure develops. During this time of decreased renal reserve and chronic renal insuffi­ciency, the client is at increased risk for acute renal failure be­cause of the diminished availability of functioning nephrons.

When renal deterioration is sudden, the capacity of the func­tioning nephrons is exceeded more quickly, and renal failure may develop with the loss of only 50% of functioning neph­rons. Acute renal failure and chronic renal failure are compared in Table 72-1. Acute renal failure affects many body systems; chronic renal failure affects every body system. The abnormal­ities are primarily related to the effects of the following:

·       Fluid volume excess

·       Electrolyte and acid-base abnormalities

·       Accumulated nitrogenous wastes

·       Hormonal inadequacies

When renal function decreases to the point where the kid­neys can no longer meet the body's homeostatic demands, renal replacement therapy is required to prevent death from po­tentially life-threatening consequences.




Acute renal failure (ARF) is a rapid decrease in renal func­tion, leading to the accumulation of metabolic waste in the body. ARF can result from conditions that cause inadequate kidney perfusion (prerenal failure); damage to the glomeruli, interstitium, or tubules (intrarenal failure); or obstruction (postrenal failure) (Kelly, 1997). ARF in clients with chronic renal insufficiency (CRI) may result in end-stage renal dis­ease (ESRD) or may resolve to nearly the pre-ARF level of re­nal function. Many factors contribute to renal insults resulting in ARF, but the acute syndrome may be reversible.


The pathophysiologic process of ARF is related to the cause of the sudden decrease in kidney function and the involved site orsites of the kidney. Hypoperfusion, toxins, tubular ischemia, infections, and obstruction have different effects on the renal system. Any of these processes can result in a decreased glomerular filtration rate (GFR), alterations in renal tubular cell membrane integrity, and tubular lumen obstruction.

With acute hypoperfusion, autoregulatory responses (i.e., renal vasoconstriction, activation of renin-angiotensin-aldosterone, and release of antidiuretic hormone [ADH]) in­crease blood volume and improve renal perfusion. However, these compensatory mechanisms cause urine volume to fall, resulting in oliguria (urine output less than 400 mL/day). Tubular cell injury is more likely to occur from the increasing ischemia related to hypoperfusion. Toxins can cause vasocon-strictive responses in the kidney, leading to reduced renal blood flow and renal ischemia.

Interstitial inflammatory changes resulting from infection, drugs, or infiltrating tumors result in immune-mediated changes in renal tissue. With extensive tubular damage, sloughing of tubular cells and other formed elements (e.g., red blood cell [RBC] casts) may obstruct the tubular lumen and prevent the formation or outflow of urine. Obstruction any­where within the genitourinary tract eventually results in full or partial obstruction to the formation and outflow of urine.

When intratubular pressure exceeds glomerular hydro­static pressure, glomerular filtration ceases. This process causes a progressive elevation of the serum blood urea nitro­gen (BUN) and creatinine levels. When the BUN rises faster than the serum creatinine level, the cause is usually related to protein catabolism or volume depletion. When both the BUN and creatinine levels rise and the ratio between the two re­mains constant, renal failure is present.



Several syndromes describe the types of ARF. These include prerenal azotemia, intrarenal (intrinsic) ARF, and postrenal azotemia. Table 72-2 summarizes the pathologic changes and causes of ARF.

Prerenal azotemia can be reversed by establishing normal intravascular volume, increasing blood pressure and cardiac output. Prolonged, untreated hypoperfusion can lead to severe ischemic injury and intrarenal failure.

The term intrarenal ARF is often shortened to just ARF in the clinical setting. Other terms include acute tubular necro­sis (ATN)and lower nephron nephrosis. Infections (bacte­ria, viral, fungal, or endotoxin), drugs (especially aminogly-coside antibiotics andnonsteroidal anti-inflammatory drugs [NSAIDs]), and infiltrating tumors (e.g., lymphomas or leukemias) can cause acute interstitial nephritis. Inflamma­tion of the glomeruli (glomerulonephritis) or of the small ves­sels of the kidneys (vasculitis) or a major obstruction to blood flow can also cause intrarenal ARF.

Postrenal azotemia develops from obstruction to the out­flow of formed urine anywhere within the genitourinary tract.


When a client's renal function has been compromised, the phases of ARF begin (Table 72-3). Increasing numbers of clients have anonoliguric form of ARF. The description of the phases of this form of ARF are similar to those described in Table 72-3 except for the references to urine output. In addi­tion, the treatment of these clients is less complicated because renal replacement therapy is rarely needed. Interventions to restore circulating volume, improve cardiac output, or re­establish blood pressure may prevent progression of the phases when renal hypoperfusion is present.


Many types of renal insults can lead to reduced renal function. Severe hypotension from excessive blood loss or dehydrationresults in hypoperfusion of blood to the kidneys and can lead to prerenal ARF. Cardiac disease or heart failure also results in decreased renal perfusion. The client may be oliguric, or even anuric (less than 100 mL/24 hr), if the dehydration or re­nal blood flow obstruction is severe. The following are other conditions that precipitate ARF:

·       Nephrotoxic agents (antibiotics, NSAIDs) (Table 72-4)

·       Disseminated intravascular coagulation (DIC)

·       Obstruction by thrombosis or stenosis

·       Uric acid crystals or other obstructing precipitates

·       Acute hemolytic transfusion reactions

·       Complications of infection (e.g., endotoxins or sepsis)

·       Acute glomerulonephritis

·       Vasculitis

·       Severe hypertension

·       Hepatorenal syndrome of cirrhosis




ARF affects 20% of all critically ill clients and carries a 50% to 80% mortality rate (Stark, 1998). Eighty percent of ARF episodes are due to ATN and exacerbations of CRI. Volume depletion leading to prerenal azotemia is the most common cause of acute renal deterioration and is reversible in most cases with prompt intervention.

For clients surviving the precipitating event, the opportu­nity for return of renal function is good. Complications dur­ing the course of ARF can vastly increase mortality. Blood­stream infections associated with central and peripheral lines and the pulmonary system are most often involved in compli­cations. However, the highest mortality occurs with trauma (70%) and surgery. ARF caused bynephrotoxic substances is associated with the lowest rates (10% to 26%) of recovery. The prognosis for ARF caused by obstruction or glomeru­lonephritis is much better.



Nurses have an essential role in the prevention of acute renal failure (ARF). The nurse notes the signs of impending renaldysfunction through careful physical assessment and close monitoring of laboratory values. Prompt recognition and cor­rection ofextrarenal problems usually restore renal function before tissue damage can occur. Careful physical assessment is required to evaluate the client's fluid status. Intake and out­put records and body weights can assist in identifying trends in fluid balance. If vascular volume is depleted, decreased urine output, postural hypotension, and tachycardia will be present. Prompt fluid resuscitation for clients in the prerenal stage can prevent intrarenal problems that can lead to renal tissue damage and renal failure.



The nurse also monitors laboratory values for any changes that reflect compromised renal function. Decreased urine spe­cific gravity indicates a loss of urine-concentrating ability and is the earliest sign of renal tubular damage. Other laboratory values that are helpful in monitoring renal function include serum creatinine, urine and serum electrolytes, and blood urea nitrogen (BUN).

The nurse is aware of nephrotoxic substances that the client may ingest or be exposed to (see Table 72-4). The nurse ques­tions orders for potentially nephrotoxic drags, and the ordered dose is validated before the client receives the drag. Antibi­otics are the most likely drag group to have nephrotoxic side effects. NSAIDs may cause or potentiate the risk for ARF. Combinations of drags can cause synergistic reactions, further increasing the risk for ARF. If a client must receive a poten­tially nephrotoxic drag, the nurse monitors laboratory values, including BUN, creatinine, and drag peak and trough levels, closely for indications of actual or potential renal dysfunction.



The accurate diagnosis of ARF, including its type and its cause, largely depends on a detailed history. The history must includequestions relating to the potential causes of ARF. The client is asked about exposure to nephrotoxins, recent surgery or trauma, transfusion, or other factors that might lead to renal is­chemia. A medication history is also important, since treatment with certain anti-infectives, aminoglycoside antibiotics, angiotensin-converting enzyme (ACE) inhibitors, and NSAIDs can cause prerenal failure. Exposure to radiographic contrast medium can precipitate ARF, especially in older clients with re­duced renal reserve. In some situations, ARF must be differen­tiated from chronic renal insufficiency (CRI). In these cases, the nurse asks about known renal diseases; systemic diseases, such as diabetes mellitus and systemic lupus erythematosus and other connective tissue diseases; and chronic hypertension.

To identify possible acute glomerulonephritis, questions about acute illnesses such as influenza, colds, gastroenteritis, and sore throats or pharyngitis, as well as the presence of cocoa-colored urine (hematuria), are included.

Reversible prerenal azotemia may be suspected after hy­potension, hemorrhage or shock, burns, congestive heart fail­ure (CHF), or any situation in which the client experiences in-travascular volume depletion. Phosphorus-containing bowel preparations and being allowed nothing by mouth (NPO) pre-operatively, in conjunction with the fluid losses of most sur­gical procedures, are sufficient to cause prerenal azotemia in many clients (Orias, Mahnensmith, & Perazella, 1999).

Postrenal azotemia can be identified by focusing on any history of obstructive disease processes that would be mani­fested as difficulty in starting the urine stream, changes in the amount or appearance of the urine, narrowing of the urine stream, nocturia, urgency, or symptoms of renal calculi. The nurse also notes any history of malignant carcinoma that may cause bilateral obstruction.

Because of the widely varied causes and the potentially re­versible nature of the illness, the nurse obtains or validates a detailed history when ARF is suspected. In clients with postrenal azotemia, the nurse monitors for oliguria or intermittent anuria, symptoms of uremia, and lethargy. The nurse reports changes in the character of the urine stream or difficulty starting urination. 


The clinical manifestations of ARF are related to azotemia, as well to as the underlying cause (Chart). Signs and symp­toms ofprerenal azotemia are hypotension, tachycardia, de­creased urine output, decreased cardiac output, decreased central venous pressure (CVP), and lethargy. The general clinical appearance of a client with prerenal azotemia is sim­ilar to that of a client with heart failure or dehydration, de­pending on the cause of the renal compromise.

Intrarenal (intrinsic) ARF usually involves damage to the glomeruli, interstitium, or tubules. Classic manifestations in­clude oliguriaor anuria (absence of urine), edema, hyperten­sion, tachycardia, shortness of breath, jugular venous disten-tion, elevated CVP, weight gain, rales or crackles, anorexia, nausea, vomiting, and lethargy or varying levels of conscious­ness. Clinical manifestations of electrolyte abnormalities, such as electrocardiographic (ECG) changes, may also be present.



The numerous alterations in laboratory values in the client with ARF are similar to those occurring in chronic renal fail­ure (CRF). The nurse can expect to find rising BUN andcreatinine levels, and abnormalities in serum electrolytes. Table 72-5 shows the effects of renal fail­ure on electrolyte values. Clients with ARF, however, typi­cally do not experience the anemia associated with CRF un; less there is hemorrhagic blood loss. However,uremic hemolysis secondary to severe azotemia can develop and may be the cause of anemia in the early phase of ARF.

In the early phases of ARF, urinalysis and microscopic ex­amination of urine may provide diagnostic information. Urine sodium levels are often less than 10 to 20 mEq/L in clients with prerenal azotemia. In prerenal azotemia, the urine is of­ten concentrated, with a specific gravity greater than 1.020. The presence of urine sediment (red blood cells [RBCs], RBC casts, tubular cells), myoglobin, or hemoglobin; a urinary sodium level lower than 40 mEq/L; and a specific gravity of 1.010 are indicative of intrarenal failure. Inpostrenal failure, urinary sodium levels may be normal to 40 mEq/L, with a specific gravity of 1.000 to 1.010.



X-ray studies help to determine the cause of ARF. A flat-plate x-ray film of the abdomen is obtained to determine the size of the kidneys. In the absence of underlying renal disease, nor­mal-size kidneys are expected. Enlarged kidneys, possibly due to obstruction, may result from hydronephrosis. This x-ray finding may also illustrate obstructing calculi in the renal pelvis, ureters, or bladder.

Renal ultrasonography is a noninvasive procedure using high-energy sound waves. It is useful in the diagnosis of uri­nary tract obstruction. Dilation of the renal calyces and col­lecting ducts, as well as calculi, can be detected.

Computed tomography (CT) scans without contrast dye can be obtained to identify obstruction or tumors. Contrast media are usually avoided to prevent further renal damage. A sonogram is generally preferred to the intravenous pyelogram (IVP) to determine kidney size and the patency of the ureters.

Aortorenal angiography may be used to examine renal blood vessels and blood flow. The procedure involves the nec­essary risk of using contrast media but can reveal any occlu­sion of major renal vessels by thrombus, embolus, or stenosis. Cystoscopy or retrograde pyelography may be indicated to identify possible obstructive lesions in the urinary tract.


Renal biopsy may be performed if the primary cause is un­certain, an immunologic disease is suspected, or the re­versibility of the renal failure needs to be determined after ARF has persisted for an extended period. The nurse assists with many of the diagnostic studies, prepares the client before the test, and provides follow-up care. The nurse must be aware of all test results and understand how they may affect the treatment regimen. (See Chapter 69 for a detailed discus­sion of renal diagnostic tests.)



The primary nursing diagnosis and collaborative problems for the client with acute renal failure (ARF) are Excess Fluid Vol­ume, Potential for Pulmonary Edema, and Potential for Elec­trolyte Imbalances. The client with ARF may pass from the oliguric phase (in which fluid and electrolytes are retained) to the diuretic phase. If the client moves to the diuretic phase, hypovolemia and electrolyteloss are the primary problems. As a result, the client in the diuretic phase of ARF needs a plan of care that focuses on fluid and electrolyte replacement and monitoring.

These examples of output variation reflect the continually changing nature of ARF and the need for the plan of care to be constantly updated to reflect the client's movement through the stages of the disease process. Drug therapy, diet therapy, and renal replacement therapy (peritoneal dialysis [PD], hemodialysis [HD], or hemofiltration) are commonly employed in the management of ARF.

DRUG THERAPY. Clients with ARF receive numerous medications. As kidney function changes, the physician often modifies drug doses. The nurse is knowledgeable about the site of drug metabolism and is especially careful when ad­ministering medications. The nurse constantly monitors for possible side effects and interactions of the drags the client with ARF is receiving. Diuretics may be used to increase urine output.

In clients with prerenal azotemia, fluid challenges and di­uretics are often used to promote renal perfusion. In clients without signs and symptoms of fluid volume excess, 500 to 1000 mL of normal saline may be infused over a 1-hour pe­riod. In prerenal azotemia, the client should respond to the fluid challenge by producing urine soon after the initial bolus. Diuretics such as furosemide (Lasix) may also be ordered in conjunction with a fluid bolus. If oliguric renal failure is diag­nosed, the fluid challenges and diuretics are discontinued. The physician may prescribe low-dose (1 to 3 |xg/kg) dopamine in a continuous infusion to enhance renal perfusion and/or in­crease blood pressure (Zellner, 1999) (Chart 72-4). These clients often require central venous pressure (CVP) monitor­ing or measurement of pulmonary arterial pressure by means of a Swan-Ganz catheter for a more exact evaluation of their hemodynamicstatus. They also require constant nursing su­pervision for assessment of the response to fluid and drug ad­ministration. The nurse carefully monitors for signs of possi­ble fluid overload.

Calcium channel blockers may be used to treat ARF re­sulting from nephrotoxic acute tubular necrosis (ATN) by pre­venting the influx of calcium into the kidney cells, thereby maintaining cell integrity and improving the glomerular fil­tration rate (GFR).

DIET THERAPY. Clients who have ARF often have a high rate of catabolism. The exact mechanism for this state is not well understood. Increases in catabolism may be related to the stress of a critical illness, causing an increase in levels of cir­culatingcatecholamines, cortisol, and glucagon, all of which stimulate catabolism. The rate of catabolism is correlated with the severity of uremia and azotemia. This hypercatabolic state causes the breakdown of muscle for protein, which leads to an increase in azotemiaand an even more elevated serum blood urea nitrogen (BUN) level.

If the client with ARF has an adequate dietary intake (see Imbalanced Nutrition: Less Than Body Requirements [Chronic Renal Failure]), nutritional support may not be necessary. The health care provider may order a con­sultation with a dietitian, who will calculate the client's caloric requirements. In conjunction with the dietitian, the health care provider will order a diet with specific levels of protein and sodium and the amount of fluids required. If the client does not require dialysis, 0.6 g/kg of body weight or 40 g/day of protein is ordered. For clients needing dialysis, the protein level needed will range from 1 to 1.5 g/kg. The amount of dietary sodium ranges from 60 to 90 mEq. In the presence of hyperkalemia, dietary potassium is restricted to 60 to 70 mEq. The amount of fluid permitted is generally cal­culated to equal the urine volume plus 500 mL. The nurse continually assesses oral intake to make certain that suffi­cient calories are consumed.




Administering Renal-Dose Dopamine

Take an accurate weight because the dose is ordered ac­cording to the client's weight.

Know the hospital's policy regarding who is responsible for calculating the rate of infusion (i.e., physician, pharma­cist, or nurse). Renal-dose dopamine is 1 to 5 //.g/kg body wt/min but is converted to mL/min for an IV infusion. Before hanging the dopamine infusion, double-check the amount of dopamine added to the solution, the total vol­ume of solution (usually 250 mL), and the calculation mil-liliters per minute.

Do not hang the dopamine infusion until all questions about the calculation are clarified. If dopamine is to be infused into a peripheral vein, be sure that the line is intact and secured. Once the infusion is started, check the client's blood pressure and pulse per hospital policy or the physician's orders, usually at least every 2 hours. Notify the physician of changes in vital signs per policy or the physician's orders.

Monitor the IV site frequently for clinical manifestations of infiltration.


If infiltration occurs, stop the infusion but do not discon­tinue the IV catheter. Prepare for phentolamine (Regitine, Rogitine*) administration through the IV catheter and subcutaneously into the infiltrated tissue.

Many clients with ARF are too ill or too anorexic to eat sufficient food. For these clients, some form of nutritional support (e.g., total parenteral nutrition [TPN] or hyperalimen-tation) must be initiated to avoid catabolism. The goals of nu­tritional support in ARF are to provide sufficient nutrients to maintain or improve nutritional status, to preserve lean body mass, to restore or maintain fluid balance, and to preserve re­nal function.

If TPN is administered, the solutions may be formulated to meet the client's specific needs. Because kidney function is unstable in ARF, the nurse constantly monitors the serum electrolyte concentrations and facilitates revisions in the hy-peralimentation solution as needed. In addition to TPN, intra­venous (IV) fat emulsion (Intralipid) infusions provide a non-protein source of calories. In uremicclients, fat emulsions can be used in place of glucose to avoid the problems associated with excessive sugars.

DIALYSIS THERAPIES. Hemodialysis (HD) and peri­toneal dialysis (PD) may be implemented for clients with ARF if necessary. Until recently, intermittent hemodialysis (IHD) has been the most common treatment of ARF. The fol­lowing are indications for dialysis in ARF:


  Persistent hyperkalemia

  Uncompensated metabolic acidosis

  Fluid volume excess unresponsive to diuretics

  Uremic pericarditis

  Uremic encephalopathy

Immediate vascular access for HD in clients with ARF is es­tablished by placement of a dual- or triple-lumen catheter specifically designed for HD. For HD that is expected to be nec­essary for several weeks, the catheter is usually placed into the subclavian or internal jugular vein. If only one or two treatments are expected to be necessary, as for removal of drugs or toxins by hemoperfusion, a femoral site may be selected. Longer use of the femoral site is generally discouraged because of position­ing limitations (i.e., required immobility) and other potential complications, such as hematomas and infection. Repeated can-nulation of the femoral site also increases the risk for hematoma formation and makes repeated use of the vein impossible.

The subclavian vein is often preferred over femoral vein cannulation because the catheter can be left in place between dialysis treatments. This placement is also a disadvantage, however, because the longer the catheter is left in place, the greater is the chance for infection. The subclavian dialysis catheter (Figure 72-1) is inserted at the bedside. A physician performs the sterile procedure, and then the catheter is cov­ered with a sterile dressing. Catheter placement is checked by chest x-ray examination before its use.

HD catheters have two lumens separating the outflow and inflow extensions of the catheter. Consequently, the continuous outflow of blood to be dialyzed is separated from the dialyzed blood returned through the inflow port and lumen. A triple-lumen catheter for HD is now available. The third lumen pro­vides a port for drawing venous blood or administering med­ication and fluid without interruption of the dialysis lumens.

PD may also be used in the treatment of ARF, but its use may be limited in the critically ill, since mechanically venti­lated clients may not be able to tolerate the accompanying ab­dominal distention, and since its use requires an intact, unin-fected abdominal cavity (Giuliano & Pysznik). PD uses the peritoneum as a semipermeable membrane for which dialysate is infused through a catheter implanted in the peri­toneum. A more complete discussion of PD is provided later in this chapter under Chronic Renal Failure).


Currently, continuous renal replacement therapies (CRRTs) have become the standard treatment for ARF. Renal replace­ment therapies in the form of hemofiltration may be better tol­erated than HD for clients who are critically ill, since rapid shifts of fluids and electrolytes associated with HD are avoided (Giuliano & Pysznik).

Continuous arteriovenous hemofiltration (CAVH) and con­tinuous arteriovenous hemodialysis and filtration (CAVHD) provide additional renal replacement therapies for clients with ARF. These procedures share some similarities with HD, but their use and indications are specific and limited.

CAVH is indicated for clients who are fluid volume over­loaded, resistant to diuretics, and hemodynamically unstable. The implementation of CAVH requires the placement of both arterial and venous catheters to provide adequate filtration sociated with the pump, but most pumps are equipped with alarms that detect air. These systems also require the use of anticoagulants, but at lower doses than needed for AV sys­tems. These procedures are performed in a critical care unit, and clients require continuous nursing care.


POSTHOSPITAL CARE. The posthospital care for a client with ARF varies widely, depending on the status of the disease when the client is discharged. The course of ARF varies, with re­covery lasting up to several months. If the renal failure is re­solving, follow-up care is often provided by a nephrologist or by the family physician in consultation with the nephrologist. On occasion, however, ARF results in permanent renal damage and the need for chronic dialysis or even transplantation. In these cases, theposthospital care may be as extensive and multifaceted as it is for any other client with chronic renal failure (CRF) (see Community-Based Care [Chronic Renal Failure]).

If the ARF is in the process of resolving, the follow-up care may involve a variety of services. Frequent medical visits arenecessary, as are routine laboratory blood and urine tests to monitor renal function. Consultation with a dietitian may be needed to modify the client's diet according to the degree of renal function and ongoing nutritional requirements. Clients continuing dialysis after discharge must be taught to limit foods high in potassium and sodium and to observe protein restrictions. In addition, education concerning the need for limited fluid intake may be necessary.

Some clients may need some form of temporary dialysis until their kidneys can metabolize fluid and waste products independently. The dialysis begun while the client was hospi­talized may be continued at an outpatient dialysis center for as long as necessary. Teaching concerning the type of dialy­sis, care of vascular access sites, dietary restrictions, fluid re­strictions, and prevention of complications is ongoing throughout the recovery phase. Depending on their level of in­dependence and family support, some clients may also need home care nursing or social work assistance.

CAVH re­moves large amounts of plasma water and solutes on a con­tinuous basis. When large volumes of plasma water are re­moved, electrolytes are also removed. Electrolytes are replaced through prescribed amounts of IV electrolyte solu­tion. The most significant disadvantage of arteriovenous (AV) filtration is the risk of bleeding associated with anticoagulants used to prevent membrane clotting (Craig, 1998).

A double-lumen dialysis catheter inserted into a large vein (subclavian, jugular) provides access for CAVHD. CAVHD uses adialysate (a solution composed of water, glucose, sodium chloride, potassium, magnesium, calcium, and bicar­bonate) delivery system to remove nitrogenous or other waste products in addition to fluid in clients with limited cardiac output, those with significant hypotension, or those who have been unresponsive to diuretic therapy. The conventional form of HD would not be tolerated, and PD would probably be in­adequate for the fluid removal required.

Continuous venovenous hemofiltration (CVVH) is often considered to be the treatment of choice for critically ill clients. CVVH requires only a double-lumen venous catheter for access and is powered by a pump, making the rate of fil­tration more reliable than that of the mean arterial pressure (Giuliano & Pysznik).



In contrast to the ability of the kidneys to regain function fol­lowing acute renal failure (ARF), chronic renal failure (CRF) represents a clinical syndrome of progressive, irreversible kid­ney injury. When kidney function is inadequate for sustaining life, CRF is referred to as end-stage renal disease (ESRD). Terms associated with renal failure include azotemia (accu­mulation of nitrogenous waste products in the bloodstream), uremia (azotemia with clinical symptoms), uremic syndrome (the diverse systemic clinical and laboratory manifestations associated with ESRD), and renal replacement therapy (hemodialysis [HD], peritoneal dialysis [PD], renal transplantation; necessary to sustain life in clients with renal failure). ARF and CRF are compared in Table.




The kidneys tend to fail in an organized fashion. The client's progression toward ESRD usually begins with a gradual de­crease in renal function of 30% to 50% (Table). Initially, there is a diminished renal reserve. A 24-hour urine specimen for monitoringcreatinine clearance is necessary to detect that renal reserve is less than normal. In this stage, reduced renal function occurs without any measurable accumulation of metabolic wastes in the serum because of the ability of the un­affected nephrons to compensate for the decreased function­ing of the diseased nephrons. Renal damage is accompanied by an elevation in the systemic blood pressure, resulting in an increase in the pressure within the glomerular apparatus and the remaining unaffected nephrons. Eventually, the unaffected nephrons may be damaged by long-term exposure to this in­creased pressure, leading to the progressive renal damage characteristic of CRF. However, under stressful conditions, such as infection, fluid overload, or dehydration, renal func­tion at this stage can appear compromised.


In the next stage, renal insufficiency, metabolic wastes be­gin to accumulate in the blood because the healthier kidney tissue can no longer compensate for the loss of nonfunction-ing nephrons. Levels of blood urea nitrogen (BUN), serum creatinine, uric acid, and phosphorus are increasingly elevated in relation to the degree of renal function loss. Careful nurs­ing and medical management of fluid volume, blood pressure, electrolytes, dietary intake, and medication administration may slow the progression of renal failure.

Many clients ultimately progress to end-stage renal dis­ease (ESRD). Excessive amounts of nitrogenous wastes, such as urea andcreatinine, accumulate in the blood, and the kidneys cannot maintain homeostasis. Initially, severe fluid over­load and electrolyte and acid-base imbalances occur. Without renal replacement therapy, fatal complications are likely.


Renal dysfunction causes multiple pathologic situations, in­cluding disruptions in the glomerular filtration rate (GFR), abnormalities of urine production and water excretion, elec­trolyte imbalances, and metabolic abnormalities. The kidneys can maintain an effective GFR until 70% to 80% of renal function is lost. Homeostasis is maintained until late in the course of renal failure. When less than 20% of the nephrons are functional, the GFR is altered despite hypertrophy of the remaining nephrons. This alteration occurs because the hy-pertrophied nephrons can maintain the excretion of solutes or waste products only by decreasing water reabsorption. As a result, hyposthenuria (the loss of urine concentrating ability) and polyuria (increased urine output) occur. Both hypos­thenuriaand polyuria are early signs of CRF and, if the prob­lem is untreated at this stage, can cause severe dehydration.

As the disease progresses, the ability to dilute the urine is increasingly diminished, resulting in urine with a fixed osmo-lality(isosthenuria). As renal function continues to diminish, the concentration of urea is increased in the blood, and urine output decreases. When renal function deteriorates to this level, the client is at risk for fluid overload because of loss of adequate urine output.


UREA AND CREATININE. Renal failure also causes disturbances in urea and creatinine excretion. Creatinine is de­rived fromcreatine and phosphocreatine, which are present in skeletal muscle. The normal rate of creatinine excretion de­pends on muscle mass, physical activity, and diet. Without ma­jor alterations in the diet or physical activity, the serum creati­nine level remains relatively constant. Creatinine is partially excreted by the renal tubules, and a decrease in renal function leads to a buildup of serum creatinine. Urea is the primary product of protein metabolism and is excreted by the kidneys. The BUN level normally varies directly with protein intake.

An important method for accurately estimating the GFR is to monitor the creatinine clearance of the kidneys. As renal function andglomerular filtration diminish, creatinine clear­ance decreases and the serum creatinine level rises (see Chapter 69).

SODIUM. In addition to decreased BUN and creatinine excretion, alterations in sodium excretion are common. Early in chronic renal failure (CRF), the client is particularly sus­ceptible to hyponatremia (sodium depletion) because, al­though a diminishing number of nephrons are reabsorbing sodium at their maximal ability, there is an obligatory loss of sodium in urine production. Thus thepolyuria often seen in early renal failure also causes sodium depletion.

In the later stages of renal failure, the capacity of the kid­neys to excrete sodium diminishes as urine production de­creases. As a result, sodium retention can occur with only modest increases in dietary sodium intake and can lead to se­vere fluid and electrolyte imbalances. Sodium retention manifests as hypertension and edema. Despite the sodium retention, the concurrent retention of water results in an apparently normal serum sodium level; di-lutional hyponatremia is likely, since fluid volume excess de­velops (see Table).

POTASSIUM. The kidney is the primary organ responsi­ble for potassium excretion. Any increase in potassium load during the later stages of renal disease can lead to hyper-kalemia (excessive potassium retention). Normal serum potas­sium levels of 3.5 to 5mEq/L are maintained until the 24-hour urine output falls below 500 mL with a decreased GFR. When hyperkalemia develops, serum levels are quickly elevated and may be 7 to 8 mEq/L or higher. Severe electrocardiographic (ECG) changes result from this elevation, increasing the risk of fatal dysrhythmias. Other factors contributing to hyper­kalemia in renal failure include ingestion of potassium in med­ications, failure to restrict potassium in the diet, excessive tis­sue breakdown secondary to the hypercatabolic state, bloodtransfusions, and excessive bleeding or hemorrhage.

ACID-BASE BALANCE. In the early stages of renal dis­ease, loss of functioning nephrons causes little change in blood pH because the remaining nephrons increase their rate of acid excretion. As the loss of nephrons continues, the kidneys can­not compensate and acid excretion is restricted; a bicarbonate deficit or metabolic acidosis results (see Chapter).

Many factors contribute to metabolic acidosis in renal fail­ure. First, the kidney becomes unable to excrete excessive hy­drogen ions. Normally, renal tubular cells secrete hydrogen ions into the tubular lumen for excretion, but ammonia and bi­carbonate are required in order for excretion to take place. In clients with renal failure, the kidney's ability to produce am­monia is decreased, and the normal reabsorption of filtered bi­carbonate does not occur. This process leads to a buildup of hydrogen ions for which the supply of bicarbonate and other buffering bases is inadequate. As a result, there is a base (bi­carbonate) deficit in an environment with excess acid. In the presence of hyperkalemia, renal ammonium production and excretion are inhibited further.

As renal failure advances and acid retention increases, res­piratory compensation is essential for maintenance of a blood pH compatible with life. The respiratory system compensates for the decreased pH by increasing the rate and depth of breathing to excrete carbon dioxide through the lungs. This pattern of breathing, called Kussmaul respiration, is in­creasingly apparent when worsening renal failure results in respiratory alkalosis. Serum bicarbonate measures the extent of metabolic acidosis (bicarbonate deficit). Individuals with CRF usually require treatment with alkali replacement to counteract acidosis.

CALCIUM AND PHOSPHATE. A complex, balanced reciprocal relationship between calcium and phosphate is in­fluenced by vitamin D (see Chapter). Vitamin D facilitates calcium absorption in the intestines, and the kidney produces 1,25-dihydroxycholecalciferol, a hormone needed to create active vitamin D.

In renal failure, phosphate retention and a deficiency of active vitamin D contribute to the disruption in calcium and phosphate balance and metabolism. Normally, excessive di­etary phosphate is excreted by the kidneys in the urine.


HYPERTENSION. Approximately 80% to 90% of clients with CRF have hypertension. Hypertension may be ei­ther the cause or the result of CRF. The elevation in blood pressure results from fluid and sodium overload and the mal­function of the renin-angiotensin-aldosterone system. The re­tention of sodium and water in renal disease causes circula­tory overload, which leads to an elevated blood pressure. The kidneys respond to a decrease in renal blood flow or low serum sodium levels by trying to improve the renal blood flow. The release of renin further stimulates the production of angiotensin and aldosterone. Angiotensin causesvasocon-striction and an elevation in blood pressure. Aldosterone, a mineralocorticoid released by the adrenal glands, stimulates the distal convoluted tubule to reabsorb sodium and water. Consequently, plasma volume is expanded, and the blood pressure is elevated. As a result of this malfunction of the renin-angiotensin-aldosterone system, the blood pressure is elevated either by vasoconstriction or by volume expansion. The kidneys do not recognize the increase in blood pressure and continue to producerenin. The result is severe hyperten­sion that is difficult to treat and that ultimately worsens renal function. Many clients with CRF also have cardiomyopathy and left ventricular hypertrophy as a consequence of pro­longed hypertension.

HYPERLIPIDEMIA. CRF is associated with alterations in the metabolism of lipoproteins. Increased triglyceride, total cholesterol, and low-density lipoprotein levels are seen with a corresponding reduction in high-density lipoprotein levels. CRF renders individuals at increased risk for coronary artery disease and acute cardiac events.

CONGESTIVE HEART FAILURE. Many clients with renal failure have some form of myocardial dysfunction. CRF causes an increased workload on the heart because of anemia, hypertension, and fluid overload. Left ventricular hypertrophy and CHF are common manifestations of late end-stage renal disease (ESRD). Uremia itself may cause uremic cardiomy­opathy, the uremic toxin effect on the myocardium. CHF is also common in these clients because of the presence of hy­pertension and coronary artery disease. Cardiac disease is the leading cause of death in clients with ESRD (U.S. Renal Data Systems, 1999).

UREMIC PERICARDITIS. Pericarditis also occurs in clients with CRF. If it is not treated effectively, this inflam­mation of the pericardium can lead to pericardial effusion, cardiac tamponade, and death. The pericardial sac becomes inflamed and irritated byuremic toxins or infection. Signs and symptoms include localized, severe chest pain, an in­creased pulse rate, a low-grade fever, and an intermittent and transient pericardial friction rub that can be heard on auscultation.

As the pericarditis continues and the pericardial effusion worsens, dysrhythmias may develop; heart tones become softer and less audible, the blood pressure decreases, and the client may experience shortness of breath. Progressive peri­cardial effusion results in cardiac tamponade, a medical and surgical emergency in which pulse pressure diminishes and bradycardia or asystole results.Treatment of pericardial tam­ponade involves removal of pericardial fluid by placement of a needle, catheter, or drainage tube into the pericardium or pericardiectomy with pericardial drainage. The incidence of uremic pericarditis has diminished with the initiation of early, aggressive dialysis.


Anemia is the primary hematologic abnormality in clients with CRF. Normochromic, normocytic anemia is a common manifestation of CRF and contributes to the client's symp­toms. The causes include a decreased erythropoietin level with resulting decreased red blood cell (RBC) production, de­creased RBC survival time resulting from uremia, iron and folic acid deficiencies, and impaired platelet function as a re­sult of uremic toxins.


Uremia can affect all levels of the gastrointestinal (GI) sys­tem. The normal flora of the oral cavity is altered in uremia. The mouth normally contains the enzyme urease, which hy-drolyzes urea. The ammonia generated from this reaction con­tributes to uremichalitosis and may also cause uremic stoma­titis (mouth inflammation).

Anorexia, nausea, vomiting, and hiccups are relatively common in clients with uremia. The specific cause of these symptoms is uncertain but may be related to increased ni­trogenous waste levels (i.e., blood urea nitrogen [BUN] and creatinine levels) and metabolic acidosis.

Peptic ulcer disease is also common in clients with uremia; however, the exact cause is unclear. Uremic colitis with pro­found watery diarrhea or constipation may also be present in clients with uremia. Ulcerations may occur in the stomach or small or large intestine, causing erosion of blood vessels. The blood loss caused by these erosions may result in melena or, in more serious cases, may progress to hemorrhagic shock from severe GI bleeding.


The etiology of CRF is complex (Table). There are more than 100 different disease processes that can result in pro­gressive loss of renal function (see also Chapter 71). How­ever, diabetes and hypertension are the most common causes of CRF.


The number of clients with CRF is continually increasing. The 1999 U.S. Renal Data Systems annual report suggests that more than 307,000 people in the United States are re­ceiving treatment for ESRD. In 1999 the reported incidence of renal disease (i.e., new clients requiring renal replacement therapy) was 79,102. There were more than 57,000 deaths in 1999 related to ESRD. Three primary causes of ESRD in­clude diabetes mellitus  (40%), hypertension (27%), and

glomerulonephritis (11%). There is a higher incidence of ESRD in men than in women (U.S. Renal Data Systems). The greatest increase in ESRD is in those 65 years of age and older. More than 221,000 people were estimated to be receiving renal replacement therapy in the United States in 1999 (U.S. Renal Data Systems, 1999). Chart addresses prevention of renal and urinary problems.






When taking a history from a client with suspected chronic renal failure (CRF), the nurse focuses on the signs and symptoms of CRF. The client's age and gender are noted. The nurse obtains accurate weight and height measurements and inquires about usual weight and recent weight gain or loss. Weight gain may indicate cardiovascular overload and fluid retention caused by poorly functioning kidneys. Weight loss may be the result of anorexia associated with the uremic syndrome. The nurse also obtains a complete history of known renal or urologic disorders, long-term health problems, medication use, and current health conditions. The client is asked about knowledge of any existing renal disease or family history of renal disease, which might indicate a hereditary disorder. A history of kidney infection or renal calculi could imply past kidney damage. It is important to explore long-term healthproblems because illnesses such as hypertension, diabetes, systemic lupus erythematosus, arthritis, cancer, and tubercu­losis can contribute to decreased renal function.

The nurse documents use of both prescription and over-the-counter medications because many medications are po­tentiallynephrotoxic and can cause renal damage.

The nurse examines the client's dietary or nutritional habits and discusses any present GI problems. A change in the taste of foods often accompanies renal failure. Clients may note that sweet foods are not as appealing or that certain foods, especially meats, leave a metallic taste in the mouth. The client is asked specifically about a history of GI prob­lems, such as nausea, vomiting, anorexia, hiccups, diarrhea, or constipation. Any of these manifestations can be the result of the buildup of nitrogenous or other metabolic wastes that the body cannot excrete because of renal malfunction.

The nurse questions the client about his or her current en­ergy level and any recent injuries or bleeding. Changes in the client's daily routine are explored as a possible result of phys­ical fatigue. Weakness, drowsiness, and shortness of breath are typical and suggest impending pulmonary edema or neu­rologic degeneration. The nurse asks specifically about ab­normal bruising or bleeding, which may be the result of hematologic changes associated with uremia.

The nurse discusses the client's urinary elimination in de­tail, including frequency of urination, appearance of the urine, and any difficulty starting or controlling urination. This infor­mation can help identify existing urologic disorders that may influence the preservation of existing renal function.


Chronic renal failure (CRF) results in many multisystem manifestations (Chart). Clinical manifestations of CRF or uremia are associated with changes in fluid volume and chemical composition. The specific causes of many of these manifestations are not known.

NEUROLOGIC MANIFESTATIONS. Neurologic man­ifestations of the uremic syndrome of CRF are numerous (see Chart) and vary widely, depending on nitrogenous waste products, acid-base imbalances, and electrolyte imbalances. The nurse observes for neurologic signs, ranging from lethargy to seizures or coma, indicating uremic encephalopathy. In addi­tion, the nurse assesses for sensory changes that generally ap­pear in a glove and stocking distribution over the lower extrem­ities and examines for weakness in the upper or lower extremities (i.e., uremic neuropathy).

If untreated, uremic encephalopathy progresses to seizures and coma. Dialysis is the treatment of choice for neurologicdisturbances associated with CRF. The manifestations of ure­mic encephalopathy resolve with the initiation of dialysis. However, improvement in uremic neuropathy is limited if the neuropathy is severe and motor function is already impaired.

CARDIOVASCULAR MANIFESTATIONS. The clini­cal manifestations of CRF and uremia lead to specific cardio­vascular abnormalities of fluid volume excess, hypertension, congestive heart failure (CHF), uremic pericarditis, and cardiac dysrhythmiasassociated with hyperkalemia. The nurse assesses for signs of a diminished ability to excrete salt and water. The resulting circulatory fluid overload, if untreated, can lead to CHF, pulmonary edema, peripheral edema, and hypertension.

The nurse assesses heart rate and rhythm, listening for ex­tra beats (particularly an S3), irregular patterns, or a pericardial friction rub. Unless a hemodialysis (HD) vascular access has been previously created, blood pressure is measured in each arm. The nurse assesses the jugular veins for distention and as­sesses for the presence of pedal, pretibial, presacral, and peri-orbital edema. Shortness of breath with exertion and paroxys­mal nocturnal dyspnea (PND) suggest fluid volume excess.

RESPIRATORY MANIFESTATIONS. Respiratory manifestations of CRF vary widely among clients (e.g., breath that smells like urine [uremic fetor or uremic halitosis], deep sighing, yawning, shortness of breath). The nurse notes the rhythm, rate, and depth of breathing. Tachypnea (increased rate of breathing) and hyperpnea (increased depth of breathing) are respiratory compensation mechanisms for worsening metabolic acidosis.

With severe metabolic acidosis, the nurse may observe ex­treme hyperventilation or Kussmaul respiration. A few clients have hilarpneumonitis, or uremic lung. In these clients, the nurse assesses for thick sputum, minimal coughing, an in­creased respiratory rate, and an elevated temperature. A pleu-ral friction rub may be heard with a stethoscope. Clients often have pleuritic pain with breathing. The nurse auscultates the lungs for crackles, which indicate fluid volume overload.

HEMATOLOGIC MANIFESTATIONS. Hematologic abnormalities include anemia and abnormal bleeding. The nurse notes indicators of anemia, including fatigue, pallor, lethargy, weakness, shortness of breath, and dizziness. The presence of abnormal bleeding is assessed by observing for bruising, petechiae, purpura, ecchymoses (confluent braises), mucous membrane bleeding in the nose or gums, abnormal vaginal bleeding, or gastrointestinal (GI) bleeding (often demonstrated by black tarry stools [melena]).

GASTROINTESTINAL       MANIFESTATIONS. The nurse assesses for a foul odor to the breath, mouth ulceration, or mouth inflammation and notes any vomiting. Abdominal pain or cramping may be associated with uremic colitis. Stools may test positive for blood.

URINARY MANIFESTATIONS. The urinary findings in renal failure reflect the kidneys' decreasing functioning. At first, changes occur in the amount, frequency, and appearance of the urine. Many etiologic features of chronic renal disease result inproteinuria; some cause hematuria.

The quantity and composition of the urine change as re­nal function deteriorates. With the onset of end-stage renal disease (ESRD), the urine may become more dilute and clearer, reflecting a diminished glomerular filtration rate (GFR). The nurse must be aware that the actual urine out­put in a client with CRF varies with the amount of remain­ing renal function. The client with ESRD usually hasoligu-ria, but some clients will remain relatively nonoliguric, producing 1 L or more per 24 hours. Urine volume pro­duced per day will probably change again after dialysis is initiated.

INTEGUMENTARY MANIFESTATIONS. There are several dermatologic manifestations of CRF. In clients with uremia, deposition of urochrome pigment in the skin results in a yellowish coloration. Some African Americans report a dark­ening of the skin. The anemia of CRF causes a sallowness to the quality of the color, which some people describe as a faded suntan. This is most noticeable in lighter-skinned clients.

Skin oils and turgor are decreased in clients with uremia. One of the most uncomfortable problems of uremia is severe pruritus(itching). The nurse also assesses for bruises (ec­chymoses), purple patches (purpura), and occasionally, drug-induced rashes.

Uremic frost, a layer of urea crystals from evaporated per­spiration, may appear on the face, eyebrows, axilla, and groin in clients with advanced uremic syndrome.


CRF and its treatment disrupt more aspects of a client's life than almost any other illness. Nurses are in a unique position to evaluate the client with newly diagnosed renal failure and to assist with these adjustments.

Psychosocial assessment and support are part of the nurse's role from the time that CRF is first diagnosed. Ini­tially, the nurse asks about the client's understanding of the diagnosis and its implications for treatment regimens (e.g., diet, medication, and dialysis). The nurse assesses for any signs of anxiety and for the coping mechanisms used by the client or family members. Some of the psychosocial aspects altered by CRF include family relations, social activity, work patterns, body image, and sexual activity. Thechronicity of ESRD, the variety of treatment options, and the uncertainties surrounding the course of the disease and its treatment neces­sitate an ongoing psychosocial assessment.


CRF results in serious abnormalities in many laboratory val­ues (see Chart). The following blood values are routinelymonitored in clients with CRF: creatinine, blood urea nitro­gen (BUN), sodium, potassium, calcium, phosphate, bicar­bonate, hemoglobin, and hematocrit.

Initially, a urinalysis is performed, and a 24-hour urine specimen for creatinine and urea clearance is obtained. In the early stages of renal insufficiency, urinalysis can reveal key indicators of kidney function. Urinalysis may show excessive protein, glucose, red blood cells (RBCs), white blood cells (WBCs), and decreased or fixed specific gravity. Urine osmo-lality is usually decreased. A 24-hourcreatinine clearance is calculated after serum and urinary creatinine levels are col­lected and quantified. These data, along with information on body weight and height, are used to calculate renal creatinine clearance. As renal failure progresses, the urine output may decrease dramatically.

Trends in renal function and progressive deterioration are typically monitored by measurements of the serum creatinine and BUN levels. Serum creatinine levels may increase gradu­ally over a period of years, reaching levels of 15 to 30 mg/dL or more, depending on the client's muscle mass. Urea nitro­gen levels are directly related to dietary protein intake. With­out dietary protein restriction, BUN levels are typically 10 to 20 times the value of the serum creatinine level. As dietary protein is increasingly restricted in an attempt to slow the rate of progression of renal failure, BUN levels remain elevated but less than the 10:1 to 20:1 ratio of nonprotein-restricted clients. Other factors affect the level of BUN, and the nurse must consider these for a complete assessment. Chapter 69 describes the factors influencing BUN levels, as well as the interpretation of serum creatinine and creatinine clearance.


X-ray findings in clients with CRF are few. Bone radio­graphs of the metacarpals and phalanges of the hand can re­veal the presence of renal osteodystrophy. With established ESRD, the kidneys are atrophic and may be 8 to 9 cm or less. This diminished size is usually the result of renal tubu­lar atrophy and fibrosis. If obstructive uropathy is a possible factor contributing to deterioration of renal function that is more rapid than expected, a renal ultrasound or computed tomography (CT) scan without contrast media may be ob­tained. (See Chapter 69 for a complete description of renal diagnostic tests.)

CRITICAL THINKING CHALLENGEYou are gathering the initial history for a 67-year-old African-American client admitted to your unit with suspected CRF. The client tells you that he has a history of diabetes, gout, and peptic ulcer disease. He also states that he has noted a 7-pound weight gain over the last 4 weeks.

  What other questions should you ask this client regarding his symptoms?

  What risk factors for the development of CRF are noted in his past medical history?

  What cardiac and respiratory manifestations may you findon physical examination of this client?


The client with chronic renal failure (CRF) has usually expe­rienced a progressive degeneration of renal function and is of­ten hospitalized for evaluation and modification of the treat­ment plan. The focus of care is to control or manage symptoms and prevent complications.


The following are priority nursing diagnoses for clients with CRF:

1.  Imbalanced Nutrition: Less Than Body Requirements related to nausea and vomiting, decreased appetite, ef­fects of a catabolic state, decreased level of conscious­ness, altered taste sensations, or dietary restrictions

2.  Excess Fluid Volume related to compromised regula­tory mechanisms (inability of the kidneys to maintain body fluid balance)

3.  Decreased Cardiac Output related to reduction in stroke volume as a result of electrical malfunction (dysrhythmias) and mechanical malfunction (increased preload [volume excess] and increased afterload [increased pe­ripheral vascular resistance])

4. Risk for Infection related to inadequate primary de­fenses (broken skin), chronic disease, or malnutrition

5.  Risk for Injury related to internal biochemical risk fac­tors associated with renal failure (increased susceptibil­ity to bleeding, falls, and pathologic fractures) and ex­ternal risk factors, such as drugs

6. Fatigue related to altered metabolic energy production, imbalance between oxygen supply and demand, and anemia

7. Anxiety related to threat to or change in health status, socioeconomic status, relationships, role functioning, support systems, or self-concept; situational crisis; threat of death; lack of knowledge (procedures, diagnostic tests, disease process, renal replacement therapy); loss of con­trol; feelings of failure; or disrupted family life

8. The primary collaborative problem is Potential for Pul­monary Edema.


In addition to the common nursing diagnoses and collabora­tive problems, clients with CRF may have one or more of thefollowing:

·       Diarrhea related to chemical or electrolyte imbalances, ear, anxiety, or side effects of medications

·       Impaired Oral Mucous Membrane related to parotid gland changes, limited fluid intake, malnutrition, and el­evated levels ofuremic toxins

·       Impaired Skin Integrity related to altered chemical bal­ance and uremic toxins

·       Social Isolation related to illness or alterations in physi­cal appearance

·       Interrupted Family Processes related to situational crisis, educed income, unemployment, or effects of chronicillness

·       Sexual Dysfunction related to altered body function (decreased libido and/or impotence) from disease and/or effects of medications, depression, or disturbance in self-esteem or body image

·       Disturbed Thought Processes related to irritation, centralnervous system (CNS) depression, side effects of med­ications, sleep deprivation, or clinical depression

·       Deficient Knowledge (disease process, care regimen,and follow-up care) related to lack of informational re­sources and magnitude of the care issues

·       Potential for Sepsis

·       Potential for Malnutrition

·       Potential for Electrolyte Imbalances

·       Potential for Metabolic Acidosis

·       Potential for Gastrointestinal (GI) Bleeding

 Planning and Implementation

The Concept Map on p. 1683 addresses assessment and nurs­ing care issues related to clients who have renal failure that has progressed to end-stage renal disease (ESRD).


PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to attain and maintain the following:

  Adequate nutritional status

  Ideal body weight for age, height, and body build

  Laboratory values within safe levels


 The nutritional requirements and dietary restrictions for the client with renal failure vary ac­cording to the degree of decrease in renal function and the type of dialysis performed, if any (Table).

 NUTRITION THERAPY. The purpose of nutrition therapy is the administration of food and fluids to support the metabolicprocesses of a client who is malnourished or at high risk of be­coming malnourished. Clients begun on hemodialysis (HD) have an increase in catabolism and subsequent decrease in in­take that often results in a loss of lean body mass. NIC inter­ventions for nutrition therapy are summarized in Chart.

The client is referred to a registered dietitian for dietary teaching and planning. The nurse in collaboration with the di­etitian instructs the client about alterations in the diet that are necessary as a result of CRF. Dietary alterations include con­trol of protein intake; limitation of fluid intake; restriction of potassium, sodium, and phosphorus intake; administration of appropriate vitamin and mineral supplements; and provision of adequate calories to meet metabolic demand.

If adequate calories are not supplied, the body will use tis­sue protein for energy, which leads to a negative nitrogen bal­ance and malnutrition. The dietitian assists in determining the number of calories and types of nutrients needed to meet nu­tritional requirements.




PROTEIN RESTRICTION. There is some evidence to suggest that early implementation of a protein-restricted diet prevents some of the symptoms associated with CRF and may preserve kidney function. Dietary protein is restricted on the basis of the degree of renal insufficiency and the severity of the symptoms in accordance with the belief that the accumu­lation of waste products from protein metabolism is the pri
àãó cause of uremia. However, recently the value of a low-protein diet has been debated. Malnutrition is often seen in clients undergoing maintenance HD, and at least one study suggests that a low-protein diet may not be necessary in renal failure. Some studies indicate that a prescription of 1.5 g of protein/kg of body weight per day may be necessary for weight gain and improvement in nutritional status in clients undergoing maintenance HD (Kuhlmann, Schmidt, & Kohler, 1999; Mehrotra &Nolph).

In clinical practice the glomerular filtration rate (GFR) is often used as an indicator of renal function and can be a guide to safe levels of protein consumption. A client with a severely reduced GFR who is not undergoing dialysis is usually per­mitted 0.55 to 0.60 g of protein per kilogram of body weight (e.g., 40 g of protein daily for a 150-pound [70-kg] adult). If proteinuria is present, protein is added to the diet in amounts equal to that lost in the urine, as determined by a 24-hour urine collection. The calculation for the protein requirement is based on actual body weight (corrected for edema), not ideal body weight.

The client receiving dialysis requires more protein because of protein loss through dialysis. HD clients have their protein requirements individually tailored according to their postdial-ysis, or "dry," weight. Typically, HD clients are allowed pro­tein in the amount of 1 to 1.5 g/kg/day; peritoneal dialysis (PD) clients are allowed 1.2 to 1.5 g/kg/day because protein is lost with each exchange (Levine). Three fourths of the protein should be of high biologic value, such as milk, meat, or eggs. If protein intake is inadequate, a negative ni­trogen balance develops and causes muscle wasting. Serum albumin and blood urea nitrogen (BUN) levels are used to monitor the adequacy of protein intake. Decreases in serum albumin levels indicate inadequate protein intake and malnu­trition. Excessive protein intake can dramatically increase BUN levels in clients with renal failure.

SODIUM RESTRICTION. The nurse monitors fluid and sodium intake. In clients with little or no urine output, fluid and sodium retention can cause edema, hypertension, and congestive heart failure (CHF). Most clients with renal failure retain sodium; a few cannot conserve sodium.

The client's status in terms of fluid and sodium retention can be estimated by monitoring body weight and blood pressure. Innondialyzed uremic clients, sodium is limited to 1 to 3 g daily, and fluid intake depends on urine output. In oliguric clients re­ceiving dialysis, the sodium restriction is 2 to 4 g daily; fluid in­take is limited to 500 to 700 mL plus the amount of any urine output. The client is instructed not to add salt at the table or dur­ing food preparation. Foods high in sodium (processed foods, fast foods, potato chips, pretzels, pickles, ham, bacon, and sausage) are permitted in moderation. Herbs and spices can be used as an alternative to salt for enhanced flavoring of food.


POTASSIUM RESTRICTION. The nurse monitors potas­sium intake because hyperkalemia can cause dangerous cardiacdysrhythmias. Cardiac rhythm is monitored for the tall, peaked T waves characteristic of hyperkalemia; the serum potassium level is also documented. The client with advanced CRF is in­structed to limit potassium intake to 60 to 70 mEq/day. The la­bels of seasoning agents are carefully inspected for sodium and potassium content. Clients are instructed to avoid salt substitute agents, many of which are composed of potassium chloride, if oliguria is present. Clients receiving PD or who are producing urine may not need dietary potassium restrictions.

PHOSPHORUS RESTRICTION. Control of phosphate lev­els is begun early in renal failure to avoid osteodystrophy. The nurse monitors serum phosphate levels, and the physician may order dietary phosphorus restrictions and medications to assist with phosphate control. Phosphate binders must be taken at mealtime. Most clients with kidney disease already restrict their protein intake, and because high-protein foods are high in phos­phorus, their phosphorus consumption is also reduced. Chapter 11 lists foods high in potassium, sodium, and phosphorus.

VITAMIN SUPPLEMENTATION. Most clients with renal failure require daily vitamin and mineral supplementation. Low-protein diets are usually deficient in vitamins, and water-soluble vitamins are removed from the blood during dialysis. In addition, anemia is a chronic problem in clients with renal failure because of the limited iron content of low-protein di­ets and decreased erythropoietin production by the kidneys. Thus supplemental iron is needed. Calcium and vitamin D supplements may also be required, depending on the client's serum levels and bone status.

INDIVIDUAUZATION OF THE DIET. Clients undergoing PD require a slightly different diet from those undergoing HD. Because protein is lost with the dialysate in PD, a major nutritional problem for these clients is replacing lost protein. In many cases, 1.2 to 1.5 g of protein per kilogram of body weight per day is recommended. The anorexia that often ac­companies advanced renal disease requires clients to consume a diet with sufficient protein that includes high-calorie enteral supplements. The amount of sodium restriction varies with fluid weight gain and blood pressure. There is usually no need to restrict dietary potassium because thedialysate is potas­sium free. The potassium restriction, if any, is determined by the serum potassium level.

The nurse plays a vital role in managing the client's diet. In collaboration with the dietitian, the nurse provides teaching and performs ongoing assessments of the client's comprehen­sion of and compliance with dietary regimens. Written exam­ples of the prescribed diet can be given to the client and fam­ily. The nurse and dietitian can help clients adapt the diet to their budget, ethnic background, and food preferences to maximize caloric intake within the diet's restrictions.


PLANNING:  EXPECTED OUTCOMES.  The client with chronic renal failure (CRF) is expected to:

  Achieve and maintain an acceptable fluid balance

  Minimize the risk of complications from fluid imbal­ances


 Management of the client with CRF includes drug therapy, diet therapy, fluid restriction, and dial­ysis. Diet therapy is discussed under Imbalanced Nutrition: Less Than Body Requirements.

 FLUID MANAGEMENT. The purpose of fluid manage­ment is the promotion of fluid balance and the prevention of complications resulting from abnormal or undesired fluid lev­els. The nurse monitors the client's intake and output and hydration status. In addition, the nurse as­sesses for signs and symptoms indicative of fluid volume ex­cess, such as crackles in the bases of the lungs, edema, and distended neck veins.

DRUG THERAPY. Diuretics are prescribed for clients with renal insufficiency when needed for treatment of fluid retention or to help control blood pressure. The diuresis pro­duced from these drugs is useful in treating fluid overload in clients who still have some urine output. Diuretics are seldom used in clients with end-stage renal disease (ESRD) after dialysis has been initiated because, as kidney function dimin­ishes, these drugs can have harmful side effects, including nephrotoxic and ototoxic effects.

The nurse uses daily weight measurements and intake and output records as important sources of assessment data. Daily weight gain generally indicates fluid retention rather than true body weight gain. The nurse estimates the amount of fluid re­tained: 1 kg of weight equals approximately 1 L of fluid re­tained. Daily weights are taken at the same time each day, on the same scale, with the client wearing the same amount of clothing, and after the bladder has been emptied if the client is not anuric. The weight is monitored for changes before and after dialysis.

FLUID RESTRICTION. The amount of fluid restriction or­dered is discussed under Sodium Restriction, p. 1684. The nurse considers all forms of intake, including oral, intra­venous, and fluid or medication administration through gas­trointestinal (GI) tubes, when calculating fluid intake. The nurse assists the client in distributing fluid intake by mouth over a 24-hour period. The client's response to fluid restric­tion is monitored, and the health care provider is notified if signs and symptoms of fluid volume excess persist or worsen.


PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to attain and maintain normal sinus rhythm, adequate cardiac output, and blood pressure in ex­pected ranges.

INTERVENTIONS. Many clients with long-standing hypertension have renal insufficiency, and some progress to CRF and ESRD. Therefore the control of hypertension is an essential factor in preserving renal function. To control hy­pertension, the physician may order calcium channel block-ers, angiotensin-converting enzyme (ACE) inhibitors, alpha-adrenergic and beta-adrenergic blockers, and vasodilators. Recent studies have documented the effectiveness of ACE in­hibitors, as compared with otherantihypertensives, in slowing the progression of renal failure (Levine, 1997). More inforation on the specific medications can be found in Chapter 36. Indications vary, depending on the client, and these drags are used carefully to avoid hyperkalemia and hypotension. Various combinations and doses may be tried until blood pressure control is adequate and side effects are minimized. Calcium channel blockers seem to improve the GFR and re­nal blood flow.

The client and family or significant others are instructed to measure blood pressure. The nurse evaluates the client's abil­ity to measure and record blood pressure accurately using the client's own equipment. The nurse periodically rechecks measurement accuracy. In addition to accurate measurement of blood pressure, the client and family must understand the relationship of blood pressure control and regulation to diet and medication therapy. The nurse further instructs the client to measure weight daily and to bring records of blood pres­sure measurements and weights for discussion with the physi­cian, nurse, or dietitian.

The nurse assesses and monitors, on an ongoing basis, for signs and symptoms of decreased cardiac output, heart fail­ure, congestive heart failure (CHF), and dysrhythmias. These topics are discussed in Chapters.


PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to remain free of infection.

INTERVENTIONS. The nurse or assistive nursing per­sonnel provides meticulous care to any areas where skin in­tegrity has been broken (incisions, site of drains, puncture sites, cracked or excoriated skin, pressure sores) and provides good basic preventive skin care. For clients undergoing dialy­sis, the nurse also inspects the vascular access site or PD catheter insertion site. These areas are assessed on an ongoing basis for redness, swelling, pain, and drainage. Vital signs are monitored for any signs or symptoms of infection.


PLANNING: EXPECTED OUTCOMES. The client with chronic renal failure (CRF) is expected to remain free of injury (will not fall or experience injury from a fall and will not experience pathologic fractures, bleeding, or toxic effects of medications administered in the presence of CRF).

INTERVENTIONS. Managing drag therapy in clients with CRF is a complex and ongoing clinical problem. Many over-the-counter drags contain ingredients that may affect renal function. Therefore it is important to obtain a detailed drag his­tory. The nurse must be aware of the use of each drag, its side effects, and the site of metabolism. The nurse, in conjunction with the physician and pharmacist, monitors the client closely for drag-related complications and adjusts dosages accordingly.

Certain medications must be avoided, and the dosages of others must be adjusted according to the degree of remaining renal function. As the client's renal function decreases, re­peated dosage adjustments are necessary. The nurse assesses for side effects and signs of drug toxicity and notifies the physician as appropriate.

A number of medications are routinely administered to clients with renal failure. The nurse giving these medications understands the rationale for administration and the nursing interventions for each drag. Many clients have some degree of cardiac disease and may require car­diotonic drags, such as digoxin. Clients with decreased renal function are particularly susceptible to digoxin toxicity be­cause the drug is excreted by the kidneys. The nurse caring for clients with CRF who are receiving any digitalis derivative, including digoxin, monitors for signs of toxicity, such as nau­sea, vomiting, anorexia, visual disturbances, restlessness, headache, fatigue, confusion, cardiac irregularities (particu­larly bradycardia [pulse rate, 50 to 60 beats/min] and tachy­cardia [pulse rate, 100 beats/min]), and serum drag levels above therapeutic range. In addition, serum levels of potas­sium are monitored closely in any client receiving cardiotonic medications.

Drags to control an excessively high phosphate level in­clude phosphate-binding compounds. Calcium acetate, cal­cium carbonate, and aluminum hydroxide are used as phosphate-binding agents in clients with renal failure. These drags treat the metabolic complications that if untreated may lead to renal osteodystrophy and related injuries. To prevent further complications, the nurse stresses the importance of these and all medications.

Hypercalcemia (excessively high serum calcium levels) is a possible complication for clients taking calcium-containing compounds to control phosphate excess. Hypophosphatemia (low serum phosphoras levels) is also a possible outcome of phosphate binding but is typically also associated with phos­phate depletion in clients who are not eating adequately but are continuing to take phosphate-binding medications. In clients taking aluminum-based phosphate binders for pro­longed periods, retention and deposition of aluminum may cause bone disease or neurologic manifestations that may not be reversible. The nurse monitors the client for evidence of muscle weakness, anorexia, malaise, tremors, or bone pain.

Clients with renal disease should avoid antacid compounds containing magnesium. Clients with renal failure cannot ex­crete magnesium and thus should avoid additional intake.

In addition to the drugs used to treat renal failure, the use of other medications requires special consideration. These medications include antibiotics, opioids, antihypertensives, diuretics, insulin, and heparin.

Many antibiotics are safe for clients with renal failure, but those excreted primarily by the kidneys require dose modifi­cation. To prevent complications of bloodstream infections from oral cavity bacteria, prophylactic antibiotic treatment is routinely given to clients with CRF before any dental proce­dures. The antibiotic and protocol used vary with the client's needs and the physician's preference.

The nurse administers opioid analgesics cautiously in clients with renal failure because the effects often last much longer than in people with healthy kidneys. Clients with ure­mia are particularly sensitive to the respiratory depressant ef­fects of these drags. Because opioids are metabolized by the liver and not the kidneys, the dose recommendations are often the same regardless of the level of renal function. The nurse monitors these clients closely after opioid administration and evaluates the need for additional administration on the basis of the client's reaction to the drag.

As renal disease progresses, the client with diabetes melli-tus often requires modification of an insulin or oral antidia-betic drag dose because of decreased insulin metabolism by ailing kidneys. Frequent blood glucose determinations are obtained to evaluate the client's insulin or oral agent needs. Urine glucose measurements are less accurate when renal dis­ease is present.

Because of poor platelet function and capillary fragility in renal failure, heparin and other anticoagulants are used cautiously.


HI PLANNING: EXPECTED OUTCOMES. The client with chronic renal failure (CRF) is expected to conserve en­ergy by balancing activity and rest in order to be able to per­form self-care and activities of daily living.

INTERVENTIONS. All clients with renal dysfunction are given some type of vitamin and mineral supplement. Be­cause of diet restrictions and vitamin losses associated with both peritoneal dialysis (PD) and hemodialysis (HD), water-soluble vitamins must be replaced. The nurse avoids giving the client these vitamin supplements before HD treatment be­cause they will be dialyzed out of the body and the client will receive no benefit.

The anemic client with CRF is treated with recombinant erythropoietin (erythropoietin alfa [Epogen, Procrit]). The goal of erythropoietin therapy is to achieve a hematocrit of 30% to 35%. For erythropoietin to stimulate bone marrow to produce red blood cells (RBCs), clients must have adequate iron stores. In addition, chronic administration of erythropoi­etin can deplete iron stores, necessitating iron supplementa­tion. Many who receive epoetin alfa report improved appetite and sexual function along with decreased fatigue; in some clients, hypertension associated with a rise in hematocrit has been reported. The improved appetite may challenge clients in their attempts to maintain dietary protein, potassium, and fluid restrictions and necessitates additional education.


PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to eliminate or reduce feelings of ap­prehension and tension from an unidentified source as evi­denced by:

Seeking information to reduce anxiety

  Using effective coping strategies

  Reporting an absence of physical manifestations of nxiety

INTERVENTIONS. The nurse has the most frequent contact with the client with CRF when the client is hospital­ized or undergoing in-center dialysis treatments. Thus nurses perform an ongoing assessment of the client's anxiety level to determine the level of nursing intervention required. The nurse observes the client's behavior for physical cues indicat­ing anxiety (e.g., an anxious facial expression or gestures and an increased pulse rate). In addition, the nurse evaluates the support systems, as evidenced by the involvement of family and friends with the client's care.

Unfamiliar settings and situations, and lack of knowledge about treatments and tests can increase the client's anxiety level. The nurse explains all procedures, tests, and treatments. The client's knowledge deficits concerning normal renal function and renal failure are identified. Evaluating the client's current knowledge avoids needless repetition during teaching sessions. The nurse provides instruction appropriate to the client's needs and ability to understand. By explaining the dis­ease process, the nurse enhances the client's acceptance and decreases anxiety.

The nurse provides continuity of care, whenever possible, to establish a consistent nurse-client relationship to decrease anxiety and promote discussions of client and family con­cerns. As the nurse-client relationship develops, the client is encouraged to discuss current problems or concerns. A multi-disciplinary team of professionals participates to provide sup­port and counseling for the client and family, often over many years of treatment.

The nurse encourages the client to ask questions and dis­cuss fears about the diagnosis of renal failure. An open at­mosphere that allows for discussion can decrease anxiety level. Nurses also facilitate discussions with family members or significant others concerning the prognosis and the poten­tial impact on the client's lifestyle.


PLANNING: EXPECTED OUTCOMES. The client with CRF is expected to remain free of pulmonary edema. A secondary outcome is to maintain optimal fluid volume bal­ance through dialysis and pharmacologic measures, thus pre­venting the onset of pulmonary edema.

INTERVENTIONS. In the client with CRF, pulmonary edema can result from either of two distinct mechanisms: left-sided heart failure or microvascular injury. In left-sided heart failure, the heart is unable to adequately eject blood from the left ventricle, leading to an increase in hydrostatic pressure. The increased pressure allows fluid to cross the capillaries into the pulmonary interstitium. Pulmonary edema can also occur from injury to the vascular endothelium or alveolar ep­ithelial cells secondary to uremia. Fluids then leak into the in­terstitial space and ultimately into the alveoli.

The nurse assesses the client for early signs of pulmonary edema, such as restlessness, heightened anxiety, tachycardia, dyspnea, and crackles that begin at the base of the lungs. As pulmonary congestion worsens, the level of fluid in the lungs rises. Auscultation will reveal increased rales, decreased air exchange, and dullness to percussion at the upper limits of fluid collection. The client may expectorate frothy, blood-tinged sputum. With further cardiac and respiratory compro­mise, the client can become diaphoretic and cyanotic.

The client who develops pulmonary edema is often admit­ted to the intensive care unit for aggressive treatment, which includes continuous cardiac monitoring. The client is placed in a high Fowler's position and given oxygen to maximize lung expansion and improve gas exchange. Drug therapy with renal failure and pulmonary edema is difficult at best because of the potential adverse effects of drugs on the kidneys. Treat­ment of pulmonary edema involves the administration of po­tent loop diuretics, such asfurosemide (Lasix). Furosemide dosing usually begins at 40 mg, administered intravenously over a 1- to 2-minute period. This dose may be repeated in 30 minutes if no response is elicited. For clients already receiv­ing maintenance doses of furosemide, an IV dose equivalent to the oral maintenance dose is given; it is doubled in 30 minutes if no response is seen (Johnson & Lalonde, 1997). Renalimpairment multiplies the risk of ototoxicity with the use of furosemide; thus IV doses are given cautiously.

Morphine sulfate 1 to 2 mg administered intravenously is usually prescribed to reduce myocardial oxygen demand by reducing ventricular preload and to provide vasodilation and sedation. The dose is adjusted to achieve the desired response, but the potential for respiratory depression exists. Therefore the nurse monitors the client's respiratory rate and blood pres­sure closely. To further decrease hydrostatic pressure, a con­tinuous infusion pump may administer a vasodilator, such as nitroglycerin. Vital signs are monitored vigilantly, since these drugs in combination may result in severe hypotension.

Nursing interventions include Foley catheter placement and frequent assessment of urine output to gauge the effectiveness of diuretic therapy. Diuresis usually begins within 5 minutes of administration of IV furosemide. Urine output is measured every 15 to 30 minutes during the acute episode and every hour thereafter until the client is stabilized. In addition, the nurse as­sesses breath and heart sounds for improvement in crackles and for the presence of an S3, indicating fluid overload.

The nurse monitors serum chemistry results for electrolyte imbalances and reports abnormalities to the appropriate health care provider so that correction of imbalances can be initiated. Continuous cardiac monitoring is initiated to iden­tify potentialdysrhythmias. Oxygen saturation levels are monitored by pulse oximetry and arterial blood gas values. The oxygen delivery system is adjusted to maintain adequate oxygen saturation levels. The nurse monitors the client for de­terioration, manifested as increasing pulmonary congestion and hypoxemia. It may be necessary to intubate the client and mechanically ventilate the lungs at this point to prevent death.

Clients with CRF are at increased risk for developing pul­monary edema, since they may present with precipitating fluid volume overload and existing cardiac compromise sec­ondary to hypertension and volume overload. Such clients are less likely to respond quickly to treatment and are more likely to develop adverse effects from pharmacologic agents as a re­sult of renal impairment. Occasionally, ultrafiltration may be used to further reduce fluid volume.

Renal Replacement Therapies

Renal replacement therapy is required only when the clinical and laboratory manifestations of renal failure present compli­cations that are potentially life threatening or that pose con­tinuing discomfort to the client. When the client can no longer be managed with conservative therapies, such as diet, med­ication, and fluid restriction, dialysis is indicated. Transplan­tation may be discussed at any time.


Hemodialysis (HD) is one of several renal replacement thera­pies used for the treatment of renal failure (Table 72-9). Dialy­sis removes excess fluids and waste products and restores chem­ical and electrolyte balance. HD involves the extracorporeal (outside of the body) passage of the client's blood through a semipermeable membrane that serves as an artificial kidney.

CLIENT SELECTION. Any client may be considered for HD therapy. Initiation of renal replacement therapy depends on the symptoms of the client, not on the creatinine clearance. Dialysis is initiated immediately for clients who exhibit the following: fluid overload refractory to diuretics, presence of pericarditis, uncontrolled hypertension, neuro­logic manifestations, and development of bleeding diathesis. More commonly, dialysis is started when clients have signs of symptom progression, such as nausea and vomiting, de­creased attention span, decreased cognition, worsening ane­mia, and pruritus (Levine, 1997).

The duration of survival after HD depends on the client's age, the cause of renal failure, and the presence of other dis­eases, such as coronary artery disease, hypertension, or dia­betes. The following are general guideline requirements for appropriate client selection:

·       Presence of fatal, irreversible renal failure when other therapies are unacceptable or ineffective

·       Absence of illnesses that would prevent or seriously complicate HD

·       Expectation of rehabilitation

·       The client's acceptance of the regimen


DIALYSIS SETTINGS. Clients may receive HD treat­ments in any of several settings, depending on specific needs. They may be dialyzed in an acute care (hospital-based) center if they have recently begun treatment or have complicating conditions that require close nursing or medical supervision. Stable clients with chronic renal failure (CRF) may be he-modialyzed in a freestanding HD center in the community hen they no longer require intensive supervision. Stable clients may participate in complete or partial self-care in an outpatient center or with in-home HD.

In-home HD offers the least disruptive form of therapy and allows for the most adaptation of the regimen to the client's lifestyle. Unfortunately, many clients cannot participate in in-home dialysis because they lack a reliable and consistent part­ner to administer the therapy and manage the dialysis ma­chine. For some clients and partners, the responsibilities of in-home dialysis are extremely stressful, so that this option is less desirable. In addition, a water treatment system must be installed in the home to provide a safe, clean water supply for the dialysis process.

Regardless of the setting for therapy, the client needs on­going nursing support and intervention to maintain this com­plex and lifesaving treatment.

PROCEDURE. The principles of HD are based on the passive transfer of toxins, which is accomplished by diffu­sion. Diffusionis the movement of molecules from an area of higher concentration to an area of lower concentration. The rate of diffusion is affected by numerous factors. Diffusion during dialysis occurs more rapidly when the membrane pores are large, there is a large surface area of membrane, the temperature of the solutions is higher, and there is a greater difference in the solute concentrations. Molecules that are too large, such as RBCs and plasma proteins, cannot pass through the membrane.

When HD is initiated, blood and dialysate flow in opposite directions from their respective sides of an enclosed semiper-meablemembrane. The dialysate is a balanced mix of elec­trolytes and water that closely resembles human plasma. On the other side of the membrane is the client's blood, which contains metabolic waste products, excess water, and excess electrolytes. During HD, the waste products move from the blood into the dialysate because of the difference in their con­centrations (diffusion). Excess water is also removed from the blood into the dialysate (osmosis). Electrolytes can move in ei­ther direction, as needed, and take some fluid with them. Potassium and sodium typically move out of the plasma into the dialysate, whereas bicarbonate and calcium move from the dialysate into the plasma. This process continues as the blood and the dialysate are circulated past the membrane for a presetlength of time. Water volume may be removed from the plasma by applying positive or negative pressure to the system.

The components of an HD system include a dialyzer, dialysate, vascular access routes, and an HD machine. The ar­tificial kidney,or dialyzer (Figure 72-3), has four compo­nents: a blood compartment, a dialysate compartment, a semi-permeable membrane, and an enclosed structure to support the membrane.

Dialysate is made from clear water and chemicals and is free of any metabolic waste products or drugs. Because bac­teria and other microorganisms are too large to pass through the membrane, dialysate does not need to be sterile. The wa­ter used in dialysate must meet specific standards, and water treatment systems are used to ensure a safe water supply. The dialysate composition may be altered according to the client's needs for treatment of electrolyte imbalances. During HD, the dialysate is warmed to approximately 100° F (37. 8° C) to in­crease the efficiency of diffusion and to prevent a decrease in blood temperature.

An essential function of an HD machine is the monitoring for potential problems, including the following:

·       Changes in dialysate temperature

·       Presence of air in the blood tubing

·       A blood leak in the dialysate compartment

·       Changes in the pressure or composition within the blood and the dialysate compartments


If any of these problems are detected, an alarm alerts the nurse. The monitoring systems protect the client from life-threatening complications that can result if these technical problems are not corrected.

All models of HD machines function, in principle, as il­lustrated in Figure 72-4. Figure 72-5 shows one type of ma­chine. The duration and frequency of HD treatments depend on the amount of metabolic waste to be cleared, the clearance capacity of thedialyzer, and the amount of fluid to be re­moved. Most dialyzers provide sufficient clearance to limit the total number of hours of dialysis to about 12 hours a week. This time is usually divided into three 4-hour treatments a week. For clients with less muscle or more ongoing urine pro­duction, two 5- to 6-hour treatments a week may be adequate. If the client gains large amounts of fluid weight, a longer treatment time may be needed to remove the fluid without hy­potension or severe side effects.

ANTICOAGULATION. To prevent blood clots from forming within the dialyzer membrane and the blood tubing, anticoagulation with heparin is necessary during HD treat­ments. Heparin, a short-acting anticoagulant, inhibits the ten­dency of blood to clot when it comes in contact with foreign surfaces. There is considerable variability among clients intheir anticoagulation response and elimination of heparin. The heparin dose must be adjusted on the basis of each client's need. Clients receiving erythropoietin may need more heparin. Heparin remains active in the body for 4 to 6 hours after administration, making the client at risk for hemorrhage dur­ing and immediately after HD treatments. The client must avoid any invasive procedures during that time. Thus the nurse monitors closely for any signs of bleeding or hemor­rhage. Clotting tendencies can be monitored during HD with a bedside machine (such as the Hemochron), by whole-blood clotting times (Lee-White clotting test), or by activated partial thromboplastin times (aPTT) during and after HD. Protamine sulfate is given as an antidote to neutralize heparin's antico­agulant activity when necessary.



VASCULAR ACCESS. For hemodialysis (HD) to be performed, a vascular access route is required (Table 72-10). Dialysis treatments necessitate the easy availability of a large amount of blood flow—at least 250 to 300 mL/min, usually for a period of 3 to 4 hours. Normally, the body cannot pro­vide this type of circulatory access without surgical revision of blood vessels.

LONG-TERM VASCULAR ACCESS. An internal access is preferred for most clients undergoing long-term HD (see Table 72-10). There are two common choices: an internal arte-riovenous (AV) fistula or an AV graft (Figure 72-6). AV fistulas are formed by connecting (anastomosis) an artery to a vein. The most commonly used vessels are the radial or brachial artery and the cephalic vein of the nondominant arm. This process increases the blood flow through the vein to 250 to 400 mL/min, the amount required for dialysis to be effective.



Some time is necessary for an AV fistula to develop, and the amount of time required for the fistula to "mature" varies. Primary AV fistulas may not be suitable for use for as long as 4 months. Therefore vascular access must be planned accord­ingly. As the fistula matures, the increased pressure of the ar­terial blood flow into the vein causes the vessel walls to thicken. This thickening increases their strength and suitabil­ity for repeated cannulation.

To obtain access to a fistula, the nurse cannulates it or in­serts two needles, one toward the venous blood flow and one toward the arterial blood flow. This procedure allows the HD machine to draw the blood out through the arterial needle and return it through the venous needle. The client may require a temporary vascular access (AV shunt or HD catheter) for HD treatments until the fistula is ready for use.

AV grafts are used when the AV fistula does not develop or when complications of the AV fistula limit continued use. Thepolytetrafluoroethylene (PTFE) graft is a synthetic material (Gore-Tex). This type of graft is commonly used in older clients undergoing HD.

PRECAUTIONS. Several precautions must be observed to ensure the functioning of an internal AV fistula or AV graft. First, the nurse assesses for adequate circulation in the fistula or graft, as well as in the distal portion of the extremity. The nurse then checks for a bruit or a thrill by auscultation or pal­pation over the access site. Repeated compression can result in the loss of the vascular access; therefore the nurse avoids taking the blood pressure in the arm with the vascular access unless absolutely necessary. The AV fistula or graft is not used for administration of IV fluids; venipuncture is avoided any­where in the arm used for HD access. Chart 72-9 lists best practices for care of the client with an HD access.

COMPLICATIONS. Complications can occur regardless of the type of access. The most common problems include thrombosis or stenosis, infection, aneurysm formation, isch­emia, and high-output heart failure.

Thrombosis, or clotting, is the most frequent complication. Some clients are more susceptible to clotting than are others and may be given anticoagulants. Surgical declotting or revi­sion of stenotic areas is typically performed in the surgical suite with the use of local anesthesia.

Most infections that occur in clients undergoing long-term HD involve the vascular access. The most common organism causing infection is Staphylococcus aureus, which can be in­troduced by punctures for dialysis access. The nurse limits the incidence of infections by using careful sterile technique be­fore needle cannulation (Table 72-11).

Aneurysms can form in any internal fistula and are caused by repeated needle punctures at the same site. Aneurysms that appear to be increasing in size may cause loss of the fistula's function and require surgical repair.

Ischemia occurs in a few clients with vascular access when the formation of the fistula causes a decrease in arterial blood flow to areas distal to the fistula. Ischemic symptoms (steal syndrome) vary from cold or numb fingers to gangrene. If the collateral circulation is inadequate, the existing fistula may need to be ligated and a new fistula created in another area for circulation to be preserved in the extremity.

The shunting of blood directly from the arterial system to the venous system, through the fistula, can cause high-output heart failure in clients with a limited cardiac reserve (see Chapter 35). This complication occurs rarely, but if it does, the fistula may need to be revised to decrease the blood flow from the arterial supply.

TEMPORARY VASCULAR ACCESS. The first type of vascular access developed was the external arteriovenous (AV) shunt(Figure 72-7; see also Table 72-10), but it is rarely

used today. To create a shunt, the surgeon places a piece of sil-icone rubber (Silastic) tubing into an artery and a second piece into an adjacent vein. The tubings are connected exter­nally to provide a readily available vascular access. The arte­rial limb is used to obtain the blood for passage through the artificial kidney (dialyzer membrane), and the venous limb is used to return the blood to the client's body after each pass through the dialyzer.

Temporary vascular access with special catheters has re­placed the use of the AV shunt for most clients requiring im­mediate HD. A catheter designed for HD may be inserted into the subclavian, internal jugular, or femoral vein if no permanent vascular access is available for use (see Dialysis Therapies, pp. 1674 and 1675). The lumens of these devices are considerably smaller than the permanent accesses, and the duration of each dialysis session is increased (usually requires 4 to 8 hours).

POSTDIALYSIS NURSING CARE. The nurse closely monitors the client immediately after dialysis and for several hours afterward for any side effects from the treatment. The more common clinical manifestations of complications in­clude hypotension, headache, nausea, malaise, vomiting, dizziness, and muscle cramps.

The nurse obtains vital signs and weight for comparison with predialysis measurements. Blood pressure and weight are expected to be reduced as a result of fluid removal. Ex­cessive hypotension may require rehydration with IV fluids, such as normal saline. The client's temperature may also be elevated, because the dialysis machine warms the blood slightly. If the temperature is elevated excessively, sepsis is suspected and a blood sample is obtained, as ordered, for cul­ture and sensitivity determinations.

The heparinization required for hemodialysis (HD) in­creases the clotting time and thus the risk for excessive bleed­ing. All invasive procedures must therefore be avoided for 4 to 6 hours after dialysis, and the nurse continually monitors the client for signs ofhemorrhage during dialysis and for 1 hour after dialysis (Chart 72-10).



COMPLICATIONS. A variety of fluid-related and in­fectious complications can occur from HD. The most com­mon complications include disequilibrium syndrome and ac­quisition of viral infections.

Dialysis disequilibrium syndrome may develop during HD or after HD has been completed. The cause is unknown but may be due to the rapid decrease in blood urea nitrogen (BUN) levels during HD. These changes in urea levels can cause cerebral edema, which leads to increased intracranial pressure. Neurologic complications can result (headache, nausea, vomiting, restlessness, decreased level of conscious­ness, seizures, coma, or death).

Early recognition by the nurse of the signs of the syndrome and appropriate treatment with anticonvulsant medications andbarbiturates may prevent a life-threatening situation. Dialysis disequilibrium syndrome may be avoided, or minimized, by in­troducing HD for short periods initially with low blood flows so that rapid changes in plasma composition are avoided.

Infectious diseases transmitted by blood transfusion are another serious complication associated with long-term HD. Two of the most serious blood-transmitted infections are hep­atitis and human immunodeficiency virus (HIV).

Hepatitis infection in clients with chronic renal failure (CRF) has decreased in recent years, paralleling the decrease in blood transfusion requirement for these clients because of the availability of erythropoietin therapy. Yet, because of the blood access and the risk of microscopic exposure, hepatitis continues to be a problem for clients undergoing HD. The hep­atitis Â virus can be transmitted through the use of contami­nated needles or instruments, by entry of contaminated blood through open wounds in the skin or mucous membranes, or through transfusion of blood contaminated with the virus.




The incubation period for acute hepatitis is 6 weeks to 6 months. Thus the nurse continually monitors the client under­going HD who is receiving frequent transfusions for signs of hepatitis virus infection (see Chapter 59).

HIV is a bloodborne and body fluid-borne virus with some potential threat to clients undergoing HD. Fortunately, the risks of HIV transmission are minimized by the consistent practice of standard precautions (blood and body fluids), rou­tine screening of donated blood for HIV, and decreased num­bers of blood transfusions for clients with end-stage renal dis­ease (ESRD). Despite this progress, however, an unknown number of clients may have already been infected with the HIV virus. Clients who have been undergoing HD and who received frequent transfusions during the early to mid-1980s are at risk for acquired immunodeficiency syndrome (AIDS) (see also Chapter).





Peritoneal dialysis (PD) takes place within the peritoneal cav­ity. PD is slower than hemodialysis (HD), however, and more time is needed for the same effect to be obtained.

CLIENT SELECTION. Most clients with chronic renal failure (CRF) can select either HD or PD. For clients who arehemodynamically unstable and for those who cannot tol­erate systemic anticoagulation, PD is less hazardous than HD. The lack of vascular access due to inadequate vessels may eliminate HD as an option. In addition, some clients with a new arteriovenous (AV) fistula receive PD while waiting for the access to mature for HD. PD is also often the treatment of choice in the older adult and pediatric popula­tions because it offers more flexibility if the client's status changes frequently.

In some relatively rare situations, PD cannot be performed, usually because of peritoneal adhesions or intra-abdominal surgery in the peritoneal cavity. In these cases, the peritoneal membrane's surface area has been reduced too much to allow for adequate dialysis exchange. In other cases, peritoneal membrane fibrosis may occur after repeated infections, which decreases membrane permeability despite adequate surface area.

PROCEDURE. The surgical insertion of a siliconized rub­ber (Silastic) catheter into the abdominal cavity is required to al­low the infusion of dialyzing fluid (dialysate) (Figure). Ac­cording to the physician's order, 1 to 2 L of dialysate is infused by gravity(fill) into the peritoneal space over a 10- to 20-minute period, according to the client's tolerance. The fluid dwells in the cavity for a specified time ordered by the physician. The fluid then flows out of the body (drain) by gravity into a drainage bag. The peritoneal outflow contains the dialysate in addition to the excess water, electrolytes, and nitrogenous waste products that have accumulated in the body. The dialyzing fluid is called peritoneal effluent on outflow. The three phases of the process (infusion, or "fill"; dwell; and outflow, or drain) are con­sidered one PD exchange. The number and frequency of PD ex­changes are prescribed by the physician, depending on the clin­ical manifestations and laboratory data.

PROCESS. PD occurs through diffusion and osmosis across the semipermeable peritoneal membrane and adjacent capillaries. The peritoneal membrane is large and porous. It allows solutes, which carry fluid with them, to move by an os­motic gradient from an area of higher concentration in the body (blood) to an area of lower concentration in the dialyz­ing fluid.

The peritoneal cavity is rich in capillaries and provides a ready access to the blood supply. The fluid and waste prod­ucts dialyzed from the client move through the blood vessel walls, the interstitial tissues, and the peritoneal membrane and are removed when the dialyzing fluid is drained from the body.

The efficiency of PD can be affected by numerous situa­tions, such as changes in the peritoneal membrane's perme­ability caused by infection or irritation, and changes in the capillary blood flow resulting from vasoconstriction, vascu­lar disease, or decreased perfusion of the peritoneum. Ex­cess water removal (ultrafiltration) in HD is accomplished by use of hydrostatic positive pressure ortransmembrane negative pressure on the dialysis machine. In PD, the amount of water removed from the client depends on theconcentration of the dialysate. Increasing the glucose con­centration of the dialysate makes the solution increasingly more hypertonic. The more hypertonic the solution, the greater the osmotic pressure for ultrafiltration and thus the greater the amount of fluid removed from the client during an exchange. The physician orders the dialysate concentra­tion on the basis of the client's fluid status.



MEDICATION ADDITIVES. Heparin may be added to the dialysate to prevent fibrin clot formation in the catheter or tubing; this intraperitoneal (IP) heparin administration is necessary only after new catheter placement or with the oc­currence of peritonitis. There is no systemic absorption of heparin with IP administration, so clotting studies are not needed.

Other agents that may be administered by the IP route in­clude potassium chloride and antibiotics. Commercially pre­pared dialysatedoes not contain potassium chloride. Some clients will need potassium chloride added to the dialysate so that the dialysate does not excessively deplete potassium from the plasma. Oral potassium supplements may be prescribed in selected clients. The physician may order IP administration of antibiotics (e.g., gentamicin, vancomycin, cephalosporins) when peritonitis is present or suspected. The combination of potassium chloride and antibiotics in the same bag of dialysate is not recommended, because chemical interactions may limit effectiveness.

TYPES OF PERITONEAL DIALYSIS. Many types of PD are available, including continuous ambulatory PD, multiple-bag continuous ambulatory PD, automated PD, in­termittent PD, and continuous-cycle PD. The selection of the type depends on the client's ability and lifestyle.


In continuous ambulatory peritoneal dialysis (CAPD), the client performs self-dialysis by infusing four 2-L exchanges of dialysateinto the peritoneal cavity, where the dialysate remains for 4 to 8 hours, 7 days a week. During the dwell period, the client can choose a continuous connect system or a disconnect system.

With the continuous connect system (straight transfer set), the dialysate bag is usually attached to the catheter by 48-inch (122-cm) tubing; the empty bag and tubing are folded and worn beneath the clothing until they are used for outflow. Af­ter draining, the client removes the bag and connects a new bag to repeat the process.

With the disconnect system (Y-transfer set), the client re­moves the connecting tubing and empty dialysate bag after in­flow and attaches a protective cap to the PD catheter junction. The disconnect system eliminates the need to wear the tubing and bag but requires opening the system two extra times with each exchange. This opening of the system increases the po­tential for contamination and infection.

With CAPD treatment, no machine is necessary, and client independence is encouraged. Theoretically, no partner is required. However, many home training programs suggest that a partner be trained in CAPD as a support for the client should illness or temporary disability occur. Devices to assist in the safe, uncontaminated connection of the tubing spike with the dialysate bag are increasingly in use. These devices can be considered for clients with impaired vision, limited manual dexterity, or decreased upper extremity strength. CAPD offers the advantage of constant removal of fluid and wastes and more nearly resembles renal function than does HD. Some clients continue to perform their own exchanges while hospitalized.

MULTIPLE-BAG CONTINUOUS AMBULATORY PERI­TONEAL DIALYSIS. For those who are unable to perform self-CAPD in the acute care setting, a multiple-bag CAPD (MB-CAPD) system allows continuation of CAPD. With MB-CAPD, a manifold of tubing connected to the dialysate and hanging on a portable pole is attached to the PD catheter by connecting tub­ing (see Figure 72-8). The nurse inflows the dialysate at the pre­scribed time, allows the dwell, and initiates the outflow for each exchange. The MB-CAPD system permits mobility for the am­bulatory client and provides for continuous PD.

AUTOMATED PERITONEAL DIALYSIS. An automated cycling machine that provides for dialysate inflow, dwell, and outflow according to preset times and volumes may be used. A warming chamber for dialysate is part of the ma­chine. Automated peritoneal dialysis (APD) may be used in the acute care setting, the outpatient dialysis center, or the client's home. The functions are performed in response to machine programming that can be individualized for the client's specific needs. A typical prescription calls for 30-minute exchanges (10/10/10 for inflow, dwell, and outflow) for a period of 8 to 10 hours. The machines have numerous safety monitors and alarms and are relatively simple to learn to use.

APD has several distinct advantages. It permits the per­formance of in-home dialysis while the client sleeps, allowing him or her to be dialysis free during waking hours. Also, be­cause the number of connections and disconnections are fewer with APD, the incidence of peritonitis has been re­duced. Finally, APD provides a means by which increased volumes of dialysis solution can be administered to clients who require higher clearances (Levine, 1997).

INTERMITTENT PERITONEAL DIALYSIS. Intermittent peritoneal dialysis (IPD) combines the principles of an os­motic pressure gradient and true dialysis. The client usually requires exchanges of 2 L of dialysate at 30- to 60-minute in­tervals, allowing 15 to 20 minutes of drain time. For most anuric clients, 30 to 40 exchanges of 2 L three times weekly are sufficient. IPD treatments can be automated or manual.

CONTINUOUS-CYCLE PERITONEAL DIALYSIS. Con­tinuous-cycle peritoneal dialysis (CCPD) also uses an auto­mated cycling machine. Exchanges occur at night while the client sleeps. The final exchange of the night is left to dwell through the day and is drained the next evening as the process is repeated. CCPD offers the advantage of 24-hour dialysis, as in CAPD, but the sterile catheter system is less often violated.

COMPLICATIONS. Complications are possible with PD, but many can be treated or prevented with careful nursing care.

PERITONITIS. The major complication of PD is peritoni­tis. The most common cause of peritonitis is contamination of the connection site during an exchange. This infection of the peritoneum is manifested by cloudy dialysate outflow (efflu­ent), fever, rebound abdominal tenderness, abdominal pain, general malaise, nausea, and vomiting.

When peritonitis is suspected, the nurse sends a specimen of the dialysate outflow for culture and sensitivity study, Gram stain, and cell count to identify the infecting organism so that an appropriate antibiotic can be ordered. Procedures for routine or periodic culturing of PD effluent vary with institutional prac­tice. In today's era of cost containment, routine practices are less likely to be the norm. Cloudy or opaque effluent is the ear­liest sign of peritonitis. Thus nursing observations are key to the detection and identification of peritonitis. The best treatment of peritonitis is prevention. The nurse must maintain meticulous sterile technique when caring for the PD catheter and when hooking up or clamping off dialysate bags (Chart 72-11).

PAIN. Pain during the inflow of dialysate is common dur­ing the first few exchanges because of peritoneal irritation; however, it disappears after a week or two. Cold dialysate ag­gravates discomfort. Thus the dialysate bags should be warmed before instillation by use of a heating pad to wrap the bag or by use of the warming chamber of the automated cy­cling machine. Microwave ovens are not recommended for the warming of dialysate because of their unpredictable warming patterns and temperatures.

EXIT SITE AND TUNNEL INFECTIONS. The normal exit site from a PD catheter should be clean, dry, and without pain or evidence of inflammation. Exit site infections (ESIs) are associated with all types of PD catheters. Such infections can be difficult to treat and can become chronic. Exit site and tun­nel infections cause increased morbidity, since they can lead to peritonitis, catheter failure, and hospitalization. Dialysate leakage and pulling or twisting of the catheter can predispose the client to ESIs. A Gram stain and culture should be per­formed when exit sites have purulent drainage.

Tunnel infections occur in the path of the catheter from the skin to the cuff. Signs of infection include redness, tender­ness, and pain. ESIs are treated with antimicrobials; however, deep cuff infections usually require catheter removal.



INSUFFICIENT FLOW OF THE DIALYSATE. Constipa­tion is the primary cause of inflow or outflow problems. To prevent constipation, the physician orders a bowel preparation before placing the PD catheter. Colon evacuation before the initiation of PD may also prevent constipation. A high-fiber diet and stool softeners are often needed for ongoing preven­tion. Other causes of inflow or outflow difficulty include kinking or clamped connection tubing, the client's position­ing, fibrin clot formation, and PD catheter migration.

Because outflow drainage is by gravity, the nurse ensures that the drainage bag is lower than the client's abdomen. The nurse inspects the connection tubing and PD system for kink­ing or twisting and rechecks to make sure that clamps are open. If inflow or outflow drainage is still inadequate, the nurse attempts to stimulate inflow or outflow by repositioning the client. Turning the client to the other side or making sure that he or she is in good body alignment may help. Having the client in a supine low-Fowler's position seems to minimize the buildup of intra-abdominal pressure. Increased intra-ab-dominal pressure that occurs in the sitting or standing posi­tion, or with coughing, contributes to leakage at the PD catheter site.

Fibrin clot formation may occur after PD catheter place­ment or with the onset of peritonitis. Careful milking of the tubing may dislodge the fibrin clot and facilitate inflow and outflow. Radiographic examination is needed to identify PD catheter migration out of the pelvic area. If migration has oc­curred, the physician repositions the PD catheter.

DIALYSATE LEAKAGE. When dialysis is initiated, small volumes of dialysate are used. It may take clients 1 to 2 weeks to tolerate a full 2-L exchange without leakage around the catheter site. Leakage tends to occur most often in obese or diabetic clients, older adults, and those on long-term steroid therapy (Levine, 1997). Dialysate leakage presents as clear fluid emitting from the catheter exit site. During this time, clients may require hemodialysis (HD) support.

OTHER COMPLICATIONS. The PD effluent (outflow drainage) is expected to be relatively clear and light yellow. The nurse notes any change in the color of the outflow. With the initial exchanges, the outflow may be bloody. The physi­cian may order several in-and-out exchanges of unwarmed dialysis solution in an effort to clear the dialysate of blood. In these cases, the client's hematocrit, pulse, and blood pres­sure are closely monitored. If the drainage return is brown, a bowel perforation must be suspected. Similarly, if the out­flow is the same color as urine and has the same glucose con­centration, a possible bladder perforation should be investi­gated. If the drainage is cloudy or opaque, an infection is suspected.

NURSING CARE DURING PERITONEAL DIALY­SIS. In the hospital setting, peritoneal dialysis (PD) is rou­tinely initiated and monitored by the nursing staff. Before the treatment, the nurse evaluates baseline vital signs, including blood pressure, apical and radial pulse rates, temperature, quality of respirations, and breath sounds. The client is weighed, always on the same scale, before beginning the pro­cedure and at least every 24 hours while receiving treatment. Baseline laboratory value determinations, such as electrolyte and glucose levels, are also essential and are repeated at least daily during the PD treatment.

During PD, the nurse continually monitors the client. Vital signs are taken regularly and recorded on a flow sheet. For the first few exchanges, the nurse records the vital signs every 15 minutes. The nurse also performs an ongoing assessment of the client for signs of respiratory distress, pain, or discomfort. The abdominal dressing around the catheter exit site is checked frequently for wetness. The nurse monitors dwell time and initiates outflow. The physician orders dwell time according to the client's needs for fluid removal and elec­trolyte balance.

For hourly exchanges, dwell time usually ranges from 20 to 40 minutes. Glucose absorption may occur in some clients, and blood glucose assessment is necessary. The outflow should be a continuous stream after the clamp is completely open. The total amount of outflow is recorded accurately af­ter each exchange. Accurate inflow and outflow records are maintained when hourly PD exchanges are done. When out­flow is less than inflow, the difference is equal to the amount absorbed or retained by the client during dialysis and should be counted as intake. For clients performing self-CAPD, or when the MB-CAPD system is used, a daily weight is used to monitor fluid status. A visual inspection of the outflow bag and daily weights may be sufficient to note the adequacy of the return.


Dialysis and transplantation are life-sustaining treatments for end-stage renal disease (ESRD); transplantation is not con­sidered a "cure." It is up to each client, in consultation with nephrology personnel, to determine which type of therapy is best suited to that client's physical condition and lifestyle. In 2001, 13,290 kidney transplants were performed. Currently, more than 48,000 people are awaiting renal transplantation in the United States alone (United Network for Organ Sharing [UNOS], 2001).

CANDIDATES. Candidates for transplantation must be free of medical problems that might increase the risks associ­ated with the procedure. The usual age range for clients un­dergoing transplantation is 2 to 70 years of age. In clients older than 70 years of age, the risk of complications increases, but clients older than 70 years of age are considered on an in­dividual basis. A thorough body systems assessment of the client is performed before the client is considered for trans­plantation (see the Legal/Ethical Issues in Health Care box at right). The process of transplantation can place a life-threat­ening stress on the cardiac system in clients with advanced, uncorrectable cardiac disease. Thus these clients are usually excluded from consideration for transplantation. Contraindi­cations for transplantation include metastatic malignant neo­plasms, chronic infection, severe cardiovascular disease unre­sponsive to treatment, and severe psychosocial problems such as chemical dependency (Bartucci, 1999). In addition, long­standing disease of the pulmonary system increases the risk of morbidity and mortality owing to respiratory tract infections after transplantation. Clients with diseases of the gastroin­testinal (GI) system may require treatment before considera­tion for transplantation. Such problems as peptic ulcer and diverticulosis can be severely aggravated by the large doses of steroids used after transplantation.

The urinary system must be completely evaluated to en­sure its ability to manage normal urine flow. Many clients with ESRD have not used their lower urinary tract for ex­tended periods, and ureteral or bladder abnormalities may re­quire surgical correction before renal transplantation.

Metabolic diseases, such as diabetes mellitus, gout, and hyperparathyroidism, cause even greater risks. These clients can still accept a renal transplant, but careful observation and management are necessary to limit complications. Other con­ditions that may complicate transplantation include malignant neoplasm and inflammatory disease. Clients with a recent his­tory of a malignant tumor are usually treated with dialysis be­cause of the shortage of donor organs, the possibility that the cancer could attack the transplanted kidney, and the limited life expectancy of these clients. In addition, the immunosup-pressive agents used after transplantation increase the risk for cancer recurrence. If more than 2 to 5 years have passed since eradication of the cancer, the client can be considered for a transplant.

Other complicating conditions are considered on an individ­ual basis, depending on the client's current health status. Renaltransplantation can be considered for most of those with ESRD and may prove to be the optimal therapy for many people (see the Evidence-Based Practice for Nursing box on p. 1698).

DONORS. The sources of donor kidneys are living donors, non-heart-beating donors (NHBDs), and cadaveric donors. The available kidneys are matched on the basis of immunologic similarity between the donor and the recipient. Living donors are most often blood relatives, but in recent years, unrelated donors have been used. NHBDs are persons declared dead by cardiopulmonary criteria. Kidneys from NHBDs are harvested immediately after death in cases where clients have previously given consent for organ donation and no longer seek active treatment or by in situ preservation in which a cool preservation solution is infused via a catheter in­serted into the abdominal aorta after death is declared. Ca­daveric donors are usually individuals who suffered irre­versible brain injury, typically as a result of trauma. This type of donor must be maintained on a ventilator and have suffi­cient cardiovascular functioning in order for the kidneys to re­main transplantable (Bartucci, 1999).

The size of the kidney is seldom a problem in adults. Pe-diatric cadaveric kidneys hypertrophy to accommodate adult needs within a few months.





Organs from living related donors (LRDs) provide the highest rates of renal graft survival (90%). Donors are usually at least 18 years old because of legal requirements and are sel­dom older than 65 years of age. General physical criteria for donors include the following:

·       Absence of systemic disease and infection

·       No history of cancer

·       Absence of hypertension and renal disease

·       Adequate renal function as evidenced by diagnostic studies

In addition, LRDs must express a clear understanding of the associated surgery and a willingness to give up a kidney. Some transplant centers also require a psychiatric evaluation to determine the motivation of the donor.

Because of advances in immunosuppressant therapy and medical management, the United Network of Organ Sharing (UNOS) reported 1-year renal transplant graft survival to be 90% for all centers in the United States (UNOS, 2001).

PREOPERATIVE CARE. Many issues must be decided before transplantation. Some issues are related to client health and others to the actual transplant procedure. The Clinical Pathway on pp. 1848-1851 highlights care needs for the client undergoing renal transplantation.

IMMUNOLOGIC STUDIES. The major barrier to success­ful renal transplantation after a suitable donor kidney is avail­able is the body's ability to identify and reject tissue that is not its own. This immunologic process attacks the transplanted kidney and renders it nonfunctional. For immunologic con­traindications to be overcome, in-depth tissue typing is done on all candidates for transplantation. These studies include simple ABO blood group typing for compatible blood trans­fusions and human leukocyte antigen (HLA) studies, as well as other tests. The HLAs have become the principal histo-compatibility system used to match transplant recipients with compatible donors. The more similar the antigens of the donor are to those of the recipient, the more likely it is that the transplant will be successful and immunologic rejection will be avoided. Research is ongoing in immunology, and new in­formation in this area could increase the success rate of organ transplantations in the future (see Chapter 20).

SURGICAL TEAM. The surgical team is a group of spe­cialists trained in transplantation procedures. The team in­cludes operating room nurses (circulating and scrub nurses), clinical nurse specialists, and preoperative nurses, as well as transplant surgeons, anesthesiologists, and nephrologists. The role of the preoperative nurse includes the following:

·       Teaching about the procedure and postoperative care

·       In-depth client assessment

·       Coordination of diagnostic tests

·       Development and implementation of treatment plans

 The transplant recipient usually requires dialysis within 24 hours of the surgery. In addition, the recipient often receives a blood transfusion before surgery. Current research favors donor-specific transfusions, in which blood from the kidney donor is transfused into the recipient. This procedure has resulted in in­creased graft survival, especially of organs from LRDs.

OPERATIVE PROCEDURES. The donor nephrec-tomy procedure varies depending on whether the donor is an NHBD,cadaveric donor, or living donor. The NHBD or ca­daveric donor nephrectomy is conducted as a sterile autopsy in the operating room. All arterial and venous vessels and as long a piece of ureter as possible are carefully preserved. Af­ter removal, the kidneys are preserved until time for implan­tation into the recipient. The technique for kidney removal from living donors requires greater surgical care and is a del­icate procedure lasting 3 to 4 hours. A flank incision is used, and care is taken to avoid scarring. Donors usually experience more pain than do recipients. They also need special nursing care and support for the psychologic adjustment to loss of a body part.

The transplantation surgery usually takes 4 to 5 hours. The transplanted kidney is usually placed in the right anterior iliac fossa(Figure 72-9) instead of the usual anatomic position. This placement allows easier anastomosis of the ureter and the renal artery and vein, and it also allows for assessment by palpation. The recipient's own nonfunctioning kidneys are not usually removed unless chronic infection in one or both kid­neys would compromise overall recovery. The client is then taken to the postanesthesia unit and then, when stable, to a designated surgical unit in the transplant center or to a critical care unit.

POSTOPERATIVE CARE. Postoperative care of the kidney transplant recipient requires that nurses be knowl­edgeable about the expected clinical findings and potential complications unique to this population. Nursing care in­cludes ongoing physical assessment with an emphasis on evaluation of renal function. The transplant recipient requires particularly close attention because the immunosuppressive drug therapy to prevent tissue rejection causes impaired heal­ing and an increased susceptibility to infection. Careful uro-logic management is essential to graft success. These clients always have a large indwelling (Foley) catheter for accuratemeasurements of urine output and decompression of the blad­der and to prevent stretch on suture and anastomosis sites on the bladder. An abrupt decrease in urine output is significant, since it can herald the onset of complications such as rejec­tion, acute tubular necrosis (ATN), thrombosis, or obstruc­tion. The urine color is carefully monitored (usually hourly). The urine is initially pink and bloody, but it gradually returns to normal over a period of several days to several weeks, de­pending on renal function. A continuous bladder irrigation is occasionally prescribed to decrease the formation of blood clots, which could increase pressure in the bladder and jeop­ardize the graft. Routine catheter care is performed to mini­mize contamination of the catheter; the nurse adheres to the agency's policy. The catheter is removed as soon as possible to avoid infection, usually 3 to 7 days postoperatively. The nurse is also responsible for obtaining daily urine tests, in­cluding urinalysis, glucose determinations, tests for the pres­ence of acetone, culture, and specific gravity measurement.



During the postoperative period, the function of the trans­planted kidney (renal graft) can result in either oliguria or di­uresis. Oliguriamay occur as a result of ischemia and ATN, rejection, or other complications. To increase urine output, the physician may order diuretics and osmotic agents, such as mannitol. The nurse and the physician carefully monitor the client's fluid status because fluid overload can cause hyper­tension, congestive heart failure (CHF), and pulmonary edema. Daily weight measurement, frequent blood pressure readings, and careful intake and output measurements are re­quired to evaluate fluid status.

Instead of oliguria, the client may have diuresis, especially with a transplanted kidney from a living related donor (LRD). The nurse carefully monitors fluid intake and output and ob­serves for electrolyte imbalances, such as hypokalemia and hyponatremia.Hypovolemia from excessive diuresis may cause hypotensive episodes. The nurse strives to prevent this situation because decreased blood pressure also decreases the oxygen and blood supply to the new kidney, which can threaten graft survival.

COMPLICATIONS. Unfortunately, numerous potential complications are associated with transplantation surgery.

REJECTION. The most common and the most threatening complication of renal transplantation is rejection. Rejection is the leading cause of graft loss. A reaction occurs between the antigens in the transplanted kidney and the antibodies and cy-totoxic T-cells in the recipient's blood. These immunologic substances treat the new kidney as a foreign invader and cause tissue destruction, thrombosis, and eventual necrosis of the kid­ney. The three types of rejection are hyperacute, acute, and chronic. Acute rejection is the most common type in the trans­plant client. It is treated with increased immunosuppressive therapy and can be reversible. Rejection can be diagnosed by clinical manifestations, a renal scan, and renal biopsy. Table 72-12 summarizes the characteristics of the three types of rejec­tion; Chapter 20 discusses their pathophysiology and treatment.

ACUTE TUBULAR NECROSIS. Prolonged preservation of cadaveric kidneys before transplantation can result in isch-emicdamage that is manifested as acute tubular necrosis (ATN). These clients usually need to be dialyzed until urine output becomes sufficient and the blood urea nitrogen (BUN) and creatinine normalize. Because ATN is often difficult to distinguish from acute rejection, clients need to undergo weekly biopsies to assess the need for further immunosup-pression if rejection is occurring.

THROMBOSIS. Thrombosis may occur during the first 2 to 3 days following transplantation. A sudden decrease in urine production or output may signal impaired perfusion re­sulting from thrombosis. Ultrasound examination of the kid­ney will reveal decreased or absent blood supply, and emer­gency surgery is required to prevent further ischemic damage or loss of the graft (Bartucci, 1999).



RENAL ARTERY STENOSIS. Stenosis of the renal artery is detected by identification of hypertension, a bruit over the arteryanastomosis site, and decreased renal function. The in­volved artery must be surgically resected and the kidney anas­tomosed to another artery. Clients with vascular complica­tions nearly always require surgical intervention. Other vascular problems include vascular leakage or thrombosis, both of which require an emergency transplant nephrectomy.

OTHER COMPLICATIONS. Other complications may in­volve the wound or genitourinary tract. Wound complications, such ashematomas, abscesses, and lymphoceles, can become a medium for infection and can place external pressure on the new kidney. Infection is a significant cause of morbidity and mortality in the transplant recipient. Prevention of infection is paramount. Strict aseptic technique and handwashing must be rigorously enforced. Because of immunosuppression, trans­plant recipients may not present with typical signs of infec­tion. Low-grade fevers, mental status changes, and vague complaints of discomfort may be present before sepsis. Nurses play a pivotal role in the early detection of infection.

Genitourinary tract complications include ureteral leakage, fistula, or obstruction; calculus formation; bladder neck con-tracture; scrotal swelling; and graft rupture. Surgical inter­vention may be required.

IMMUNOSUPPRESSIVE   DRUG   THERAPY. The success of renal transplantation depends on changing the client's immunologic response so that the new kidney is not rejected as a foreign organ. The nurse administers and is aware of the immunosuppressive drugs that protect the trans­planted organ. These drugs include corticosteroids, antilym-phocyte preparations, monoclonal antibodies, and cy-closporine (Cyclosporin A). Chapter 20 discusses the mechanisms of action for these agents and the associated client responses. Clients who must take immunosuppressant medications are vulnerable to infection secondary tomyelo-suppression. Clients are at risk for developing a number of fa­tal viral, fungal, bacterial, or protozoal infections (Giuliano & Sims, 1999).

Community-Based Care


Because of the complex nature of chronic renal failure (CRF), its progressive course, and multiple treatment modalities, a case manager may be useful in the planning, coordination, and evaluation of care. As the renal disease progresses, the client is seen by a physician or nurse practitioner regularly and may have frequent hospitalizations. The nurse, in con­junction with the dietitian and social worker, evaluates the home environment and determines special equipment needs before discharge. Once the client is discharged, home care nurses may direct care and monitor progress Chart 72-12 pro­vides a focused assessment guideline for the client after renal transplantation.

The nurse provides ongoing health teaching about the diet in renal disease and the pathophysiologic process of renal dis­ease. As CRF approaches end-stage renal disease (ESRD), one of the following courses of treatment is chosen: he-modialysis (HD), peritoneal dialysis (PD), or transplantation. For each form of treatment, the client must learn the relevant information and procedures and consider his or her personal lifestyle, support systems, and methods of coping. Decision making about the treatment modality, or even whether to pur­sue treatment, is very difficult for many clients and their fam­ilies. Nurses provide information and emotional support to as­sist clients with these decisions.

Treatment with HD necessitates a working knowledge of the dialysis machine and the care of the client's vascular ac­cess. If the client chooses in-home HD, the home care nurse makes preparations for installation of the appropriate equip­ment, including a water treatment system. Regardless of whether the treatment is provided at home or in a center, the nurse provides ongoing physical assessment and health teach­ing to promote maximal independence at home.



The client receiving PD needs extensive training in the procedure. The client also needs assistance in obtaining equipment and the numerous supplies involved. Home care nurses perform physical assessments, monitor vital signs, as­sess compliance with drug and diet regimens, and carefully monitor for signs and symptoms of peritonitis.

The nurse plays a vital role in the long-term care of the client with a renal transplant. This client is usually discharged 3 to 4 weeks after surgery. Meticulous maintenance of pre­scribed immunosuppressive drug therapy is essential for the survival of the renal graft. Thus the nurse facilitates accept­ance and understanding of this regimen as a part of daily life. The nurse also carefully monitors for signs of graft rejection and for complications, such as infection.


Health teaching is a primary function of nurses caring for clients with any form of renal disease. The home care nurse collaborates with other members of the health care team, es­pecially the dietitian, pharmacist, and physician, to instruct clients and family members or significant others in all aspects of diet therapy, necessary drag therapy, and associated renal pathologic changes. Clients and family members are taught to report signs and symptoms of complications, such as fluid overload and infection. When a client requires a more ad­vanced form of therapy, such as dialysis or transplantation, the teaching focuses on the chosen therapeutic intervention.

HD is the most complex form of therapy for the client and family to understand. Even if clients receive HD in a dialysis center instead of at home, they are usually expected to have some knowledge of the HD machine. The client or a family member or other caregiver must be taught to care for the vas­cular access and to report signs of infection and stenosis. The client who plans to have in-home HD will need a partner. Both the client and the partner must be completely educated in the entire process of HD and must be able to perform it in­dependently before the client is discharged from the HD cen­ter or hospital HD unit.

PD involves extensive health teaching. This instruction can be given to the client alone or to the client and a family mem­ber or other caregiver if the client cannot perform the proce­dure. The nurse emphasizes sterile technique because peritoni­tis is the most common complication of PD performed at home. The nurse instructs clients to report the signs and symptoms as­sociated with peritonitis. They should report the presence of cloudy effluent and abdominal pain, especially when accompa­nied by rebound tenderness. Clients are taught that cloudy ef­fluent needs to be analyzed promptly. A specimen is sent by the home care nurse for culture and sensitivity, cell count, and Gram stain to identify the causative organism. Clients are taught that peritonitis is treated with antimicrobial therapy, usu­ally given by the intraperitoneal (IP) route. To prevent peritoni­tis, they are taught how breaks in aseptic technique can occur, resulting in peritonitis. In addition, to eradicate the infection, nurses must educate clients about the importance of completing the antibiotic regimen. Nurses need to teach that repeated episodes of peritonitis can result in diminished ultrafiltrationcapability, which may necessitate transfer to HD.

The client receiving a renal transplant also needs extensive health teaching. The nurse provides instruction about drug regimens, home monitoring, immunosuppression, signs and symptoms of rejection, infection, and prescribed changes in the diet and activity level.


The nurse provides psychologic support for the client and family or significant others. The nurse facilitates the client's adjustment to the diagnosis of renal failure and eventual ac­ceptance of the treatment regimens.

For many clients, the reduction of uremic symptoms in the initial weeks and months of dialysis treatment creates a sense of euphoria and well-being (the "honeymoon" period). They feel better physically, their mood may be happy and hopeful, and they tend to overlook the inconvenience and discomfort of frequent dialysis treatments. The nurse realizes that this mood is temporary and uses the time to initiate health care teaching. The nurse stresses that although the client's uremic symptoms have diminished, the client will not return com­pletely to the previous state of well-being. The client and the family may have looked on dialysis as a cure instead of a re­quired lifelong treatment. Many clients enter a phase of discouragement and disillu­sionment sometime during the first year of treatment; this may last a few months to a year or longer. The difficulties of incor­porating dialysis into daily life are staggering, and clients often become disappointed and depressed as the problems become apparent. During this time, they may struggle against the idea of having to be permanently dependent on a disruptive therapy. The fear of rejection by health staff and family members or sig­nificant others reinforces feelings of helplessness and depend­ence. Some people retreat into complete or partial denial of the disease and the need for treatment. They may deny the need for dialysis or may not comply with medication administration and dietary restrictions. Nurses who work with these clients need to monitor any maladaptive behaviors that may contribute to non-compliance and suggest psychiatric referrals. Nurses and fam­ily members should focus on the positive aspects of the treat­ments. The nurse continues health care education with clients as active participants and decision makers.

Most clients with chronic renal failure (CRF) eventually enter a phase of acceptance or, at least, resolution. The prospect of a chronic illness may be devastating for some peo­ple, and each person reacts differently. To make this long-term adaptation, the client must adjust to continuous change, but specific concerns depend on the current physical status and particular treatment method.

After clients have accepted or become resigned to the chronicity of their disease, they usually attempt to return to their previous activities. Resuming the previous level of ac­tivity, however, may not be possible. The nurse and other health care professionals can help clients to establish realistic goals that allow them to lead active, productive lives.


Professionals from various disciplines are valuable resources for the client with renal failure. Home care nurses are often required to monitor the client's status and evaluate mainte­nance of the prescribed treatment regimen (HD or PD). A client with advanced renal failure may need the assistance of a home care aide in performing the activities of daily living. Social services personnel are usually involved because of the complex process of applying for financial aid to pay for the required medical care (see the Cost of Care box above). To in­crease the functional capacity of the client, a physical thera­pist may be beneficial. Consultation with a dietitian will assist the client and family members in understanding the special dietary needs. A psychiatric evaluation may be needed to as­sist with depressive symptoms and maladjustment. Clergy and pastoral care specialists offer spiritual support.

Clients with CRF are routinely observed by a physician, usually a nephrologist. Such organizations as the National Kid­ney Foundation (NKF), the American Kidney Fund, and the National Association of Patients on Hemodialysis and Trans­plantation (NAPHT) may be helpful to clients and families.

 Evaluation: Outcomes

The nurse evaluates the care of the client with chronic re­nal failure (CRF) on the basis of the identified nursing diag­noses and collaborative problems. The expected outcomes are that the client will:

·       Achieve and maintain appropriate fluid volume

·       Maintain serum electrolyte levels in expected ranges

·       Maintain heart rate and blood pressure in expected ranges

·       Comply with the prescribed dietary regimen

·       Maintain an adequate nutritional status

·       Seek information to reduce anxiety

·       Use effective coping strategies

·       Report an absence of physical manifestations of anxiety