Medicine

Lesson 3

Lesson 3

 

Urinary Stones

 

 

Archeologic studies show that urinary tract stone disease was an affliction of humans earlier than 4800 bc (Shattock, 1905). Ancient Greek and Roman physi­cians recorded the symptoms and treatment of urologic stone disease, but little attention was directed to lo­calization of the stone or to the cause of its formation. For a complete review of the historical aspects of urinary stone disease, see Resnick and Boyce (1979).

In the 20th century, advances in technology and microscopic techniques have led to a better under­standing of the structural characteristics of calculi, their chemical composition, and the various compo­nents of urine. Many theories have been proposed to explain the cause and development of urologic calculi, but none have been able to answer fully the questions concerning stone formation. In all probability, stone disease will be found to result from the interaction of multiple factors, many of which are as yet unknown.

Theories of Stone Formation

A. Nucleation Theory: Stone formation is initi­ated by the presence of a crystal or foreign body in urine supersaturated with a crystallizing salt that favors growth of a crystal lattice.

B. Stone Matrix Theory: An organic matrix of serum and urinary proteins (albumin; a\- and 0:2-globulins and occasionally -γ-globulins; mucoproteins; and matrix substance A) provides a framework for deposition of crystals.

C. Inhibitor of Crystallization Theory: Some urinary substances, eg, magnesium, pyrophosphate, citrate, phosphocitrate, diphosphonate, mucoproteins, and various peptides, inhibit crystal formation. Ab­sence or low concentration of inhibitors permits crys­tallization.

Most investigators acknowledge that these 3 theories describe the 3 basic factors influencing uri­nary stone formation. It is likely that more than one factor operates in causing stone disease. A generalized model of stone formation combining these 3 basic theories has been proposed. A period of abnormal crystalluria is required during which large crystals or aggregates of crystals are produced in the urine. In order for these crystals to continue to grow and propa­gate, a certain number of chemical factors must be present, ie, the urine must be supersaturated with thesalt of the stone-forming crystal, certain inhibitors of crystallization must be reduced or absent from the urine, and a certain concentration of nucleating matrix material must be present.

Additional risk factors can influence the degree and severity of clinical stone disease. These include the metabolic state of the patient, which is influenced by genetic background as well as the presence of cer­tain hormonal imbalances; environmental factors, which could lead to supersaturation of already satu­rated urine; dietary excesses; and anatomic abnor­malities, which could lead to chronic infection or actu­ally enhance the deposition of crystals in the upper urinary tract.

Anatomic Site of Stone Formation

There are several different theories as to where stone formation occurs in the kidney: (1) deposition of calcium on the basement membrane of collecting tubules and on the surface of papillae; (2) deposition of linear precipitates of calcium within the renal lym­phatics to produce obstruction and breakdown of the membrane separating the lymphatics from the collect­ing tubules; and (3) intratubular deposits of amorphous necrotic calcific cellular debris or organized mi-crocalculi (or both).

DIAGNOSTIC EVALUATION            

                                                                            

Medical History

A personal as well as a family history should be obtained for all patients. A history of inflammatory bowel disease, recurrent urinary tract infection, pro­longed periods of immobilization, gout, or familial occurrence of certain inherited renal diseases, eg, renal tubular acidosis or cystinuria, should be sought. Cal­cium oxalate stone disease is inherited in a multifactorial manner, and hypercalciuria has been shown to be inherited as an autosomal dominant trait. The presence of other endocrine or metabolic disorders should also be considered.

A complete list of all medications taken should be obtained. Acetazolamide, useful in the treatment of glaucoma, has been implicated as a cause of calcium stones. Absorbable silicates, usually found as part of an antacid preparation, may rarely be implicated in the formation of silicon calculi. Ascorbic acid in amounts greater than 2 g/d may increase urinary excretion of oxalate and contribute to formation of calcium oxalate stones. Any drug that decreases the urinary pH may contribute to the formation of uric acid stones. Orthophosphates prescribed to decrease calcium stone formation have been associated with an increase in the size of struvite stones. The diuretic hydrochlorothiazide may cause uricosuria and formation of uric acid stones, and allopurinol, a potent xanthine oxidase inhibitor useful in the treatment of gout, may also cause precipitation and formation of xanthine stones in certain individuals. In patients with a history of stone disease, all methods of previous treatment, including surgery, should be documented and details of stone composition sought.

 

Symptoms & Signs at Presentation

It is generally accepted that renal stones are initi­ally formed in the proximal urinary tract and pass progressively into the calices, renal pelvis, and ureter. Their presentation may therefore vary from an inciden­tal opaque shadow found on x-ray to fulminant pyelonephrosis if obstruction and infection have oc­curred.

A. Symptoms Related to Stones at Specific Sites:

1. Caliceal stones-Small, asymptomatic, nonobstructing caliceal stones are usually discovered as incidental findings on radiograms obtained for the evaluation of other organ systems. Patients with nonobstructing caliceal stones are often asymptomatic but may consult the physician after an episode of gross hematuria. If the stone becomes large enough to obstruct an infundibulum, flank pain, recurrent infec­tion, or persistent hematuria may result.

2. Renal pelvic stones-A small stone in the renal pelvis may remain there asymptomatically, pass into the ureter, or become impacted at the ureteropelvic junction.                                    

 

                        

 

If obstruction occurs at the level of the ureteropelvic junction, the pain may be intermittent, corresponding to the obstruction of urine flow, and may be localized to the flank or the costovertebral angle. When urinary infection accompanies obstruc­tion, the patient may present with florid pyelonephritis or gram-negative septicemia.

3. Proximal ureteral stones-A calculus small enough to pass into the ureter can produce ureteral colic and hematuria. Beyond the ureteropelvic junc­tion, the ureter assumes a diameter of about 10 mm (30F), and small calculi can easily pass to the level at which the ureter crosses over the iliac vessels. At this point, the diameter of the ureter narrows to about 4 mm (12F), and stones at this level commonly obstruct urine flow. The patient who presents with a stone in the upper ureter will frequently experience a sharp, spasmodic pain of acute onset, localized to the flank. As the stone passes down the ureter to the level of the pelvic brim, the pain remains sharp and intermittent, corresponding to peristalsis of the ureter. The pain frequently will radiate to the lateral flank and abdominal area and may be accompanied by nausea and vomit­ing. The pain is typically intermittent, with intense episodic intervals followed by periods of relief (' 'renal colic").

 

            Plain film

                      

4. Distal ureteral stones-As the stone passes into the distal ureter, the pain remains intermittent and sharp, corresponding to the intermittence of ureteral peristalsis. In males, the pain frequently radiates along the inguinal canal into the groin and corresponding testicle. In females, the pain may radiate to the labia.

A third area of ureteral narrowing exists at the level of the ureterovesical junction. At this point, the ureter narrows to a diameter of 1 -5 mm and it is here that most stones become lodged. Once a calculus reaches the distal ureter and approaches the bladder, symptoms of vesical irritation frequently are noted.

 

B. Associated Nonrenal Symptoms: Owing to the arrangement of the autonomic nervous system, which transmits visceral pain, and the similar neuro­logic innervation of the kidneys and stomach by the celiac ganglia, it is not unusual for ureteral colic to be accompanied by nausea and vomit­ing. Abdominal distention resulting from reflex ileus or intestinal stasis may also be present and confuse the diagnosis. It is therefore necessary to consider other pathologic entities that may mimic the presentation of a ureteral stone. Among these are gastroenteritis, acute appendicitis, colitis, diverticulitis, salpingitis, and cholecystitis.

 

C. Variability of Symptoms: Less frequently, the passage of a stone may not be as dramatic as noted above. Such patients may describe a ' 'dull'' ache in the flank area that may have been present for several weeks without interfering with their daily routine. This pain is not as localized as acute colic and may be confused with other visceral pain.

Other less dramatic forms of presentation include persistent hematuria, either gross or microscopic, and persistent urinary tract infection. These patients will frequently have a struvite stone (see below).

Patients with asymptomatic stone disease may present initially for the evaluation of hypertension, azotemia, or symptoms referable to the gastrointestinal tract.

 

D. Findings on Physical Examination: A thorough physical examination is an essential part of the initial evaluation of the patient who may have a urinary calculus. Upon presentation to the emergency room, most patients will be experiencing severe colic and will be in obvious distress. In contradistinction to patients with acute peritonitis or abdominal pain, pa­tients with ureteral colic will toss about and be unable to find comfort in any position. Diaphoresis, tachycar­dia, and tachypnea are frequent signs. Hypertension secondary to the discomfort may also be present. Fever is usually not present unless infection is associated with obstruction.

The abdomen should be examined carefully, with particular attention directed to palpation of the flank, where ureteral obstruction may produce acutely a hy-dronephrotic kidney. The kidney or the costovertebral angle is frequently tender to palpation. The abdomen should be carefully palpated to rule out surgical causes of abdominal pain. It is not unusual for the bowel sounds to be hypoactive and for an ileus to be present on radiographic examination. The bladder should also be palpated, since urinary retention can occur second­ary to acute ureteral colic.

 

 

 

 

 

 

 

 

 

 

 

E. Laboratory Findings:                                                         

                                                      

 

   Urinalysis and urine culture are required for all patients in whom stone disease is suspected. Microscopic or gross hematuria is frequently present in patients with acute ureteral colic. However, the absence of hematuria does not rule out renal stone disease. Pyuria may be present even with­out urinary tract infection, and bacteriuria is frequently seen in female patients with acute stone disease. Find­ings suggestive of infection may alter the therapeutic approach. The presence of crystals should also be noted, since they often occur in the acute phase of stone disease and may accurately reveal the type of stone present. Urinary pH should be noted, because patients with uric acid or cystine stones usually have acidic urine and those with struvite stones have alkaline urine.

 

 

 

F. Radiographic Findings:

 

             Plain film

 Plain film (coral stoun)

 

At least 90% of all renal stones are radiopaque and therefore readily visi­ble on a plain film of the abdomen. Stones composed of calcium phosphate (apatite) are the most radiopaque and have a density similar to that of bone. Calcium oxalate is slightly less dense, followed by magnesium ammonium phosphate (struvite) and cystine. Stones composed solely of uric acid or matrix are considered to be radiolucent and would not appear on a plain film of the abdomen. Other calcifications that may appear on the plain film and be confused with a urinary calculus include calcified mesenteric lymph nodes, calcium in rib cartilage, gallstones, foreign bodies (pills), and pelvic phleboliths. Oblique films may show whether the calcification is in line with the normal anatomic position of the kidney or ureter.

1. Intravenous urography-

 

             Intravenous urogram

 

Patients whose his­tory and physical examination are compatible with urinary stone disease should undergo an intravenous urogram unless they are allergic to the contrast medium. In a patient with acute ureteral colic, the most common finding on intravenous urography is a delay in visualization of the collecting system on the affected side. In the absence of complete ureteral obstruction or a nonfunctional kidney, a dense nephrogram will ap­pear, followed by visualization of the collecting sys­tem. Delayed films should be obtained until the complete collecting system is opacified down to the area of ureteral obstruction. Frequently, stones located in the intramural portion of the ureter may be obscured by dye collected in the bladder. An oblique film ob­tained after voiding will often show the calculus.

 

2. Tomography-In patients who present with acute ureteral colic, the plain film of the abdomen often shows a paralytic ileus that may obscure existing calculi. Plain-film tomograms may help to identify a stone otherwise obscured by overlying gas or feces.

It is not uncommon to see perirenal or periureteral extravasation of contrast medium in patients with obstructing ureteral calculi. The extravasation is be­lieved to originate from a forniceal tear and is as­sociated with the increased pressure caused by the obstructing stones. In the absence of infection, the condition is self-limiting and does not require further therapy. If infection is suspected, antibiotic therapy should be instituted.

3. Retrograde urography-

 

                            Retrograde pneumopyelography  

Retrograde urograms are rarely needed to diagnose a stone; however, they are indicated when the diagnosis is suspect or the patient is allergic to contrast medium.

4. Ultrasonography-

                                

In patients in whom it is not possible to obtain an intravenous urogram, ul­trasonic evaluation of the kidneys may aid in the diag­nosis of renal stones. In pregnant women with flank pain in whom it is desirable to limit radiation exposure or in anuric patients or patients with chronic renal failure, the presence of hydronephrosis on acoustic shadowing may be diagnostic.

 

 

5. CT scanning- CT scanning is seldom indi­cated as the first diagnostic study for the evaluation of a patient with a suspected urinary calculus. However, in cases where the presence of a nonopaque stone or a urinary tract tumor is being considered, CT scans have proved diagnostic.

 

Although a radiolucent stone cannot be detected on the plain film alone, the diagnosis should be sus­pected when hydronephrosis and a radiolucent filling defect are found on sonograms or urograms.

A CT
scan may help to differentiate a stone from a blood clot or tumor.         

 

 

 

 

SURGICAL TREATMENT OF RENAL STONES                       

Renal stones that must be surgically removed may be located in the pelvis, infundibula, calices, or com­binations thereof, and specific techniques are required to manage each of these situations so as to effectively remove all stone fragments and maximally preserve renal tissue.

 

 

                           

 

Indications for surgical removal of urinary stones confined to the upper collecting system include intrac­table urinary tract infection, progressive renal damage, urinary obstruction, and persistent pain. In most cases, surgery can be delayed until a metabolic evaluation is completed. However, if severe obstruction or sepsis occurs, urinary drainage should be provided by place­ment of a ureteral catheter or by percutaneous nephrostomy.

 

      

Percutaneous nephrostomy

 

Hypothermia in Urologic Surgery

Hypothermia reduces renal metabolism and pre­vents cellular damage during periods of ischemia as­sociated with intraoperative occlusion of the renal ar­tery. Renal cooling reduces cellular metabolic activity, so that the parenchyma! cells, especially those of the proximal convoluted tubule, are better able to tolerate ischemia. The temperature needed to prevent ischemic changes is controversial, but experimental studies and clinical experience indicate that the kidney is optimally protected when it is maintained at approximately 15-20 °C. Packing the kidney in an ice slush prepared from physiologic salt solutions, applying external cooling coils, and other methods are acceptable ways of cooling the kidney.

 

Intraoperative X-Rays

Intraoperative x-rays as well as sonograms ob­tained using portable ultrasonographic equipment greatly aid the urologist in locating and removing small stone fragments. Intraoperative nephroscopy and pul­satile irrigation are also helpful in the removal of small stone fragments.

 

Open Surgical Procedures

A. Nephrectomy and Partial Nephrectomy:

Nephrectomy meets many objectives of surgery for removal of stones but cannot be endorsed for treatment of stone disease, because renal tissue is needlessly sacrificed. Indiscriminate partial nephrectomy often sacrifices salvageable renal tissue and should be per­formed only in patients with severe obstruction and parenchymal damage in whom the recovery of renal function of that segment is expected to be minimal.

 

 

   Nephrectomy

 

 

 

 

 

          Partial Nephrectomy

  

 

 

 

 

 

B. Pyelolithotomy:

 

                          Pyelolithotomy

 Simple pyelolithotomy is used for removal of calculi confined to the renal pelvis. Minimal dissection of the renal sinus is usually needed, and exposure of the entire kidney is not re­quired. This procedure is not indicated for the removal of entrapped caliceal stones or large, branched renal calculi.

C. Extended Pyelolithotomy: Trapped caliceal and branched stones usually cannot be adequately re­moved through a simple pyelotomy. Dissection of the renal sinus and exposure of the infundibula permit access to larger stones. Advocates of extended pyelo­lithotomy consider it superior to anatrophic nephro-lithotomy because it is less traumatic to the renal parenchyma. Operative blood loss is usually minimal, so that occlusion of the renal vessels is rarely required.

D. Pyelonephrolithotomy: The removal of branched calculi located within the lower pole infun-dibulum may be facilitated by extending a routine pyelotomy incision through the renal parenchyma overlying the lower pole infundibulum posteriorly. This procedure is also indicated for the removal of stones in the lower pole of a kidney with a small intrarenal renal pelvis. The procedure is relatively bloodless, and clamping of the renal artery is usually not necessary.

E. Coagulum Pyelolithotomy: Coagulum pyelolithotomy consists of use of a mixture of pooled human fibrinogen and thrombin to form a clot within the renal collecting system that effectively traps stones and facilitates their removal. The mixture is injected into the renal pelvis before the latter is opened. The renal pelvis is opened after 10 minutes, when the clot has formed. The main application of this technique is in the removal of multiple small calculi in a large extrarenal renal pelvis. It may also be useful in the removal of soft calculi that are likely to crumble during removal.

F. Anatrophic Nephrolithotomy: Intersegmental anatrophic nephrolithotomy (Boyce procedure; Smith and Boyce, 1967) is indicated for the removal of multiple or branched calculi associated with infundibu­lar stenosis. It is also indicated in situations where pyelolithotomy is technically impossible, eg, in a kid­ney with a small intrarenal renal pelvis and in cases where prior surgery has obliterated access to the renal sinus.

 

 

        Nephrolithotomy

 

 An incision is made within the avascular plane or division between the anterior and posterior vascular segments, the renal artery is clamped, and the kidney is cooled to prevent ischemic changes. When the proce­dure is properly performed, large renal calculi can be easily removed with minimal trauma to the kidney. Reconstruction of the collecting system should also be done to facilitate drainage and reduce the incidence of recurrent stone formation.

G. Radial Nephrotomy: Radial nephrotomy may be used as a primary procedure or in conjunction with any of the other surgical procedures discussed above. It is indicated for the removal of a solitary caliceal stone or a caliceal stone associated with a larger intrapelvic stone. In order to decrease in-traoperative blood loss, it is helpful to clamp the main renal artery and cool the kidney. The radial paren-chymal incisions should be made on the convex border of the posterior surface whenever possible, thereby minimizing damage to the intralobar vessels.

H. Ex Vivo, or "Bench," Surgery and Auto-transplantation: Nearly all patients with renal stone disease can be successfully managed by one of the above surgical procedures. However, "bench" surgery with autotransplantation of the kidney may have a role in treatment of patients with recurrent stone disease and a history of multiple surgical procedures, stenosis of the pelvis or proximal ureter, or calculi associated with congenital renal anomalies or of pa­tients with intractable ureteral colic.

 

 

 

 

PERCUTANEOUS STONE REMOVAL

 

                                             Percutaneous stone removal

 

Cooperative efforts between urologists and radi­ologists have led to the development of endourology. A nephroscope may be inserted through a nephrostomy tract to remove a stone from the renal pelvis. An ultrasound probe may be used to fragment a staghorn calculus.

The advantages of percutaneous methods are ob­vious. No incision is required, and many of the procedures can be performed under local anesthesia. Recov­ery time is shortened, and the patient can usually return to full activity in a short period of time.

Disadvantages include the occasional need for nephrostomy drainage for up to several weeks and the possibility of bleeding secondary to percutaneous stone manipulation. These are new techniques, and longterm effects are still uncertain, as is the success rate compared with that of more conventional surgical methods.

The criteria for percutaneous stone removal are identical to those for open procedures for stone re­moval. Patients should have complete laboratory studies, and all stones should be identified and located preoperatively. Antimicrobial drugs should be used to treat urinary tract infections before stone manipula­tion.

The cornerstone of percutaneous manipulative procedures is the placement of a percutaneous nephros­tomy tube and the establishment of a nephrostomy tube tract of adequate caliber to accommodate the nephro­scope. Immediate dilation of the nephrostomy tract and delayed dilation of the tract over a 1- to 2-week period have both been successfully employed.

The methods of stone removal are varied, and the choice is based on the experience of the surgeon and the needs of the patient. Stones can be grasped or flushed out under fluoroscopic control or under direct vision using a nephroscope. Stone baskets or specially designed forceps may be employed. Large stones may be fragmented using either an ultrasonic or electrohy-draulic lithotrite under direct vision.

The success rate for these stone removal proce­dures is greatest with renal pelvic and caliceal stones, approaching 100% in some instances. Stones impacted at the ureteropelvic junction are more difficult to re­move by these techniques; the success rate is only about 50%. Stones less than 1.5 cm in diameter can usually be removed in a single session, whereas larger stones may require multiple operative sessions. With experienced operators, the complications have thus far been limited.

 

 

TREATMENT OF RENAL STONES BY EXTRACORPOREAL SHOCK-WAVE LITHOTRIPSY

 

 

 

Extracorporeal shock-wave lithotripsy permits removal of renal stones without direct surgical inter­vention (Chaussy, 1981; Chaussy, Brendel, and Schmidt, 1980). The patient is given an epidural or general anesthetic and lowered into a tank of water at the bottom of which is placed the shock-wave elec­trode used to produce the shock waves that fragment the renal stone. The shock waves produced by the electrode are focused and directed at the stone by a 2-dimensional radiographic scanning system and are keyed to follow the R wave of the patient's ECG. The average patient receives 1000-1500 shock-wave pulses. After about 200 pulses, the stone begins to fragment. Small particles are passed in the urine over the next several days.

In studies performed on dogs, the shock waves caused no tissue damage except to the lungs, but the dosage was 50 times greater than that used on humans. The shock waves did not damage bone tissue, because of the large protein matrix of bone.

This technique is contraindicated in the presence of urinary tract obstruction or radiolucent stones.

Of 206 patients who had 221 shock-wave applica­tions, fewer than 1 % required open surgical removal of stones and 88.5% were rendered stone-free. Only 20% required analgesia after the treatment, and most were discharged after 4 days of hospitalization (Chaussy, 1981).

The only shock-wave unit presently available is in Munich. Several major institutions in the USA have ordered the instruments and will institute clinical trials. With time and further clinical experience, the indications and applications of this technique will be­come apparent.

 

TREATMENT OF URETERAL STONES

 

Ureteral stones originate in the renal collecting system and pass into the ureter, where they frequently become lodged and cause symptoms of ureteral colic. The right and left ureters are involved with equal frequency. Management depends on the size and location of the stone, age of the patient, presence or absence of urinary tract infection, anatomy of the urinary tract, and degree of symptoms. Treat­ment may be expectant, manipulative, or surgical.

Studies have shown that 31-93% of ureteral stones pass spontaneously. Size and location of the stone need to be considered when planning a course of therapy. Ninety percent of stones located in the distal ureter and measuring less than 4 mm in diameter were found to pass spontaneously, whereas only 50% of stones 4-5.9 mm in diameter passed spontaneously. Only 20% of stones greater than 6 mm in diameter passed without surgical intervention. Stones located in the proximal ureter are much less likely to pass spon­taneously.

Expectant Therapy

Most ureteral stones are less than 5 mm in diame­ter and pass spontaneously. Expectant management consists of hydration and the liberal use of analgesics. Patients are instructed to strain all urine and to save the stone for analysis. Plain films of the abdomen and pelvis are obtained at 1- to 2-week intervals to monitor progress of the stone down the ureter. If the patient develops fever associated with a urinary tract infec­tion, severe ureteral colic unresponsive to oral medica­tions, severe nausea and vomiting, complete obstruc­tion of a solitary kidney, or impaction of the stone, hospital admission and surgical or manipulative treat­ment are indicated.

Manipulative Treatment

In the past, it was generally accepted that stone manipulation should not be attempted when the stone was above the rim of the bony pelvis (Anderson, 1974). With the use of fluoroscopy to guide stone extraction, small stones lodged in the upper and mid ureter may be safely approached endoscopically with double-balloon stone catheters and a ureteroscope.

 

 

     Ureteroscopy

 

Large stones in the renal pelvis or proximal ureter have been removed using the ureteroscope and ultrasonic lithotriptor to disintegrate impacted stones. Stones 5-8 mm in diameter usually pass into the distal ureter to lodge at the ureterovesical junction; this location is ideal for transurethral manipulation.

 

               Baskets

 

                 

 

Instruments used with varying success for the removal of ureteral stones include Councill and Johnson baskets, expandable Robinson baskets, re­tractable Dormia and Pfister-Schwartz baskets, end-loop and side-loop Davis catheters, balloon catheters including double-balloon catheters, and multiple ure­teral catheters. Success rates vary according to the skill of the surgeon and the instrument used. There is a reported 93% success rate when the loop catheter is used and allowed to pass spontaneously. Wire stone baskets have been successful in about 60-70% of cases.

Complications resulting from stone manipulation are relatively rare and range from 0.3% with loop catheters to 2% with wire stone baskets. Complica­tions include urinary tract infection, hematuria, ure­teral perforation, breakage and entrapment of the stone basket, and complete avulsion of the ureter.

 

 

 

Ureteral stones have been successfully removed via percutaneous routes. Preliminary suc­cess in using the shock-wave machine to fragment upper ureteral calculi has also been reported.

 

 

 

 

Surgical Measures

 

                       Ureterolithotomy

 

Stones larger than 8 mm in diameter usually re­quire surgical intervention. Other indications for operative stone removal include the development of urinary sepsis, stones impacted anywhere in the ureter, unsuccessful attempts at stone manipulation, and physical abnormalities that do not allow stone manipu­lation, ie, urethral stricture. A number of different approaches to the ureter have been described, includ­ing the modified dorsal lumbar approach or the anterior kidney incision for stones located in the proximal ure­ter. Midureteral stones may be approached by a McBurney or Gibson incision, while stones in the distal ureter may bejemoved through a Pfannenstiel or lower midline incision. In carefully selected patients, the transvesical or transvaginal approach may be use­ful in removing distal ureteral calculi.

 

 Ureterolithotomy

 

 

 

 

 

 

BLADDER STONES

 

Primary stones of the bladder are relatively rare in the USA but occur commonly in children in parts of India, Indonesia, the Middle East, and China. These stones usually occur in sterile urine. They are uncom­mon in girls. It is believed that the incidence is related to diets low in protein and phosphate. Dehydration due to hot weather and diarrhea further compounds the problem. In areas where bladder stones are endemic, they are usually composed of ammonium acid urate.

 Benign Prostatic Hyperplasia

 

Secondary vesical stones form as a result of other urologic conditions. They nearly always occur in men and are frequently associated with urinary stasis and chronic urinary tract infection. Urinary obstruction may be due to prostatic hyperplasia or urethral stric­ture. Neurogenic vesical dysfunction may be a cause of chronic infection and urinary retention with eventual stone formation. Patients with chronic indwelling catheters frequently develop encrustations on the cath­eter and bladder calculi. Ureteral stones may pass into the bladder but fail to pass through the urethra. Foreign bodies in the urinary tract may act as a nidus for calcium deposition and stone formation.

 

 Foreign bodies in the urinary tract

 

 

 

 

Diagnostic Evaluation

Patients with bladder stones frequently give a history of hesitancy, frequency, dysuria, hematuria, dribbling, or chronic urinary tract infection unrespon-'sive to antimicrobial drug therapy. Sudden interrup­tion of the urinary stream associated with the acute onset of pain radiating down and along the penis may occur when the stone intermittently obstructs the blad­der neck.

 

        Plain film of the pelvis

 

 

 

 

         Retrograde pneumocystography

 

Most vesical stones are radiopaque and apparent on a plain film of the pelvis. Oblique films may be helpful in differentiating bladder stones from calcifications in ovaries, lymph nodes, or uterine fi­broids

 

 

             Cystoscopy

 

 

Cystoscopy is the most accurate means of diag­nosis.

Treatment

Small bladder stones may be removed by trans-urethral irrigation. Larger stones may be crushed by one of a variety of different manual lithotrites and removed from the bladder by irrigation. Ultrasonic and electrohydraulic lithotriptors are available to fragment large bladder calculi.

 

             Cystolithotomy

 

 

 

 

 Cystolithotomy

  

Stones that are too large to manage transurethrally and stones associated with prostatic hypertrophy should be removed by a suprapubic surgical procedure which allows for contemporaneous prostatectomy. Other urologic conditions that contribute to formation of stones must be corrected if recurrence is to be prevented. Chemolysis using hemiacidrin or Suby's solution G administered via a catheter may be an effec­tive form of treatment in patients who cannot tolerate general anesthetics.

 

URETHRAL STONES

 

Primary urethral calculi are formed in the urethra and are rare. They are usually found in association with an abnormality of the lower urinary tract that typically causes stasis of urine or chronic urinary tract infection and leads to stone formation. Patients with urethral diverticula, strictures, foreign bodies in the urethra, chronic urethral fistulas, benign prostatic hyperplasia, and meatal stenosis are more prone to the development of urethral stones.

Secondary urethral calculi are more common; they are formed in the kidney or bladder and become lodged in the urethra as they progress down the urinary tract.

Most urethral calculi (59-63%) are located in the anterior urethra and up to 11 % at the fossa navicularis. However, up to 42% may become impacted at the membranous urethra or external urinary sphincter.

Diagnostic Evaluation

A urethral calculus should be considered when there is a history of acute urinary retention preceded by sharp perinea! pain. Careful palpation of the urethra may disclose the presence of a pendulous or distal urethral stone. In females, the stone should be evident from transvaginal palpation of the urethra. Retrograde urethrography in males will identify the presence and location of the stone.

Treatment

Management of impacted urethral stones is surgi­cal. Therapeutic goals should include not only removal of the stone but also repair of any urethral abnormality leading to stone formation.

 

 

 

 

 

 

HYDRONEPHROSIS & NEPHROPTOSIS

 

HYDRONEPHROSIS

                 

Hydronephrosis (hydronephrotic degeneration, hydronephrotic atrophy) is a permanent progression of dilation of the pelvico-caliceal system, followed by the atrophy of the renal parenchyma and its dysfunction, caused by the urine passage disorder.

Ethiology and pathogenesis. Hydronephrosis develops owing to construction of the pelvic-urethral system, high coming out of the ureter, construction of the ureter by blood vessels, embrional fascicles, abdominal adhesions, etc.

Depending on the reason of development, are differed:

a) Hydronephrosis caused by the obstacle of the pelvic-urethral segment;

b) Obstacle within the ureter;

c) Obstacle at the lower ureter;

d) Neurogenic disorders.

The pressure within the renal pelvis is normally close to zero. When this pressure increases because of obstruction or reflux, the pelvis and calices dilate. The degree of hydronephrosis that develops depends upon the duration, degree, and site of the obstruction. The higher the obstruction, the greater the effect upon the kidney. If the renal pelvis is entirely intrarenal and the obstruction is at the ureteropelvic junction, all the pressure will be exerted upon the parenchyma. If the renal pelvis is extrarenal, only part of the pressure produced by a ureteropelvic stenosis will be extender on the parenchyma; this is because the extrarenal renal pelvis is embedded in fat and dilates more readily, thus “decompressing” the calices.

 

                       

  

In the earlier stages, the pelvic musculature undergoes compensatory hypertrophy in its effort to force urine past the obstruction. Later, however, the muscle becomes stretched and atonic (and decompensated).

The progression of hydronephrotic atrophy is as follows:

1) The earliest changes in the development of hydronephrosis are seen in the calices. The end of a normal calyx (as seen on urograms) is concave because of the papilla that projects into it; with increase in intrapelvic pressure, the fornices become blunt and rounded. With persistence of increased intrapelvic pressure, the papilla becomes flattened, then convex (clubbed) as a result of compression enhanced by ischemic atrophy. The parenchyma between the calices is affected to a lesser extent. The changes in the renal parenchyma are due to (1) compression atrophy from increase in intrapelvic pressure (more accentuated with intrarenal pelvis) and (2) ischemic atrophy from hemodynamic changes, mainly manifested in arcuate vessels that run at the base of the pyramids parallel to the kidney outline and are more vulnerable to compression between the renal capsule and the centrally increasing intrapelvic pressure.

This spotty atrophy is caused by the nature of the blood supply of the kidney. The arterioles are “end arteries”, therefore, ischemic is most marked in the areas farthest from the interlobular arteries. As the backpressure increases, hydronephrosis progresses, with the cells nearest the main arteries exhibiting the greatest resistance.

This increased pressure is transmitted up the tubules. The tubule become dilated and there cells atrophy from ischemia.

It should be pointed out that a few instances of dilated renal pelvis and calices are not due to the presence of obstruction. Rarely, the renal cavities are congenitally capacious and thus simulate hydronephrosis. More commonly, hydronephrosis may occur in childhood due to the backpressure associated with vesicoureteral reflux. If the valvular incompetence resolves (and this is common), some degree of the hydronephrotic changes may persist. These persisting changes may cause the physician to suspect the presence of obstruction, which may lead to unnecessary surgery. An isotope renogram or the Whitaker test can be performed to determine whether organic obstruction is present.

2) Only in unilateral hydronephrosis are the advanced stages of hydronephrotic atrophy seen. Eventually the kidney is completely destroyed and appears as a thin-walled sac filled with clear fluid (water and electrolytes) or pus.

 

            

 

If obstruction is unilateral, the increases intrarenal pressure will cause some suppression of renal function on that side. The closer the intrapelvic pressure approaches the glomerular filtration pressure (6-12 mm Hg), the less urine can be secreted. Glomerular filtration rate and renal plasma flow are reduced, concentrating power is gradually lost, and the urea: creatinine concentration ratio of urine from the hydronephrotic kidney is lower than that of urine from the normal kidney.

Classification. Hydronephrosis is primary or congenital, that develops because of congenital obstacle of the ureter.

Secondary hydronephrosis arises as a complication of any other disease (urinary stones of kidney or ureter, pedunculitis, tumors of kidney).

Hydronephrotic atrophy may be uni- or bilateral, aseptic and infected, opened, closed and intermitted.

There are 3 stages of the disease. The 1st stage reflects pyeloectasy (dilation just of the renal kidney with a moderate dysfunction).

II – prehydronephrosis (hydrocalicosis – the broadening of the renal pelvis and calices, thinning of the parenchyma with expressed dysfunction.

III stage – hydronephrotic atrophy, atonic of the renal pelvis. This stage means degeneration of kidney into great hollowed sack with fluid, volume up to 2 and more.

The renal tissue preserves as a slim strip along the conveyed surface, semi-lunar in shape. The number of nephrones is sharply decreased, glomeruli are deformed. Cells of the nephrones tubes are vacuolated, granular and liquid degeneration is present, even necrobiosis and necrosis somewhere. Capsules of the glomeruli are thickened due to collagen fibrosis (sclerosis).

Micro- and macroarchitectonics of the kidney is rather degenerated; compensative hyperemia is typical for the first stage. It is followed by lengthening and narrowing of the vessels, ischemia. Dystrophy of the nervous system is observed.

 

  Hydronephrosis

 

If one kidney is damaged due to hydronephrotic atrophy, the second one is enlarged in result of compensative adopting process to provide homeostasis. Infecting leads to terminal damage of the kidney.

 

Clinical signs. There are no specific symptoms of hydronephrosis. Aseptic unilateral hydronephrotic atrophy is continuously asymptomate.

Course of the disease is circulating. The intensity of signs depends on the stage of urinary tract constriction presence, activity of the infection, etc. The pain in loin is frequent. Its intensity depends on stage of structure of the urinary tract and infection activity. It may be dull, intermitting, renal colic, permanent, ache.

Renal colic is observed in case of initial hydronephrotic atrophy; dull pain and feeling of swelling appears while cumulating of urine within the kidney. The kidney is palpable, enlarged and painful while renal colic attacks.

If colic is cupped off, ache is still present for some time, but kidney isn’t palpable. This intermittent filling of kidney with the urine and its emptying may occur without pain, especially in children. Parents may notice swelling of the loin, that disappears. Ache often is followed by hematuria, fever. Therefore, hematuria may be the only sign of hydronephrosis.

 

   Plain film (Renal concrement)

 

Renal concrements cause activation of hydronephrosis clinical signs, progress of atrophy and sclerosis. Stone forms due to urine congestion and retardation of its passage.

Rather significant hydronephrosis, especially in children, may defigurate the abdomen. The kidney may be palpated as a large, mobile cyst, lying lower than common location. It is elastically resistant, with smooth surface, painful.

Frequent complication is acute or chronic pyelonephritis. Hydronephrosis, that is complicated with pyelonephritis, manifests in acute pain, fever, nausea, vomiting, sometimes – elevation of the blood pressure rate.

The significant hydronephrosis may be ruptured because of trauma.

Diagnosis.

Laboratory findings. Anemia may be found secondary to chronic infection or in advanced bilateral hydronephrosis (stage of uremia). Leukocytosis is to be expected in the acute stage of infection. Little if any elevation of the white blood count accompanies the chronic stage. Large amounts of protein are usually not found in the obstructive uropathies. Casts are not common from hydronephrotic kidneys. Microscopic hematuria may indicate renal or vesical infection, tumor, or stone. Pus cells and bacteria may or may not be present.

In the presence of unilateral hydronephrosis, results of the PSP test will be normal because of the contrlateral renal hypertrophy. Suppression of PSP excretion indicates bilateral renal damage, residual urine (vesical or bilateral ureterorenal), or vesicoureteral reflux.

In the presence of significant bilateral hydronephrosis, urine flow through the renal tubules is slowed. Thus, urea is significantly reabsorbed but creatinine is not. Blood chemistry therefore reveals a urea: creatinine ratio well above the normal 10:1.

X-ray findings.

 

              Plain film

 

 A plain film of the abdomen mayshow enlargement of renal shadows, calcific bodies suggesting ureteral or renal stone, or tumor metastases to the bones of the spine or pelvis. Metastases in the spine may be the cause of spinal cord damage (neuropathic bladder); if they are osteoblastic, they are almost certainly from cancer of the prostate.

 

 

 

 

 

      Excretory urograms

 

Excretory urograms will reveal almost the entire story unless renal function is severely impaired. They are more informative when obstruction is present because the radiopaque material is retained. These urograms will demonstrate the degree of dilatation of the pelvis, calices, and ureters. The point of ureteral stenosis will be revealed. Segmental dilatation of the lower end of a ureter implies the possibility of vesicoureteral reflux, which can be revealed by cystography.

 

 

       Retrograde cystography

 

The cystogramm may show trabeculation as an irregularity of the vesical outline and may show diverticula. Vesical tumors, nonopaque stones, and large intravesical prostatic lobes may cause radiolucent shadows. A film taken immediately after voiding will show residual urine. Few tests that are as simple and inexpensive give the physician so much information.

Retrograde cystography shows changes of the bladder wall caused by distal obstruction (trabeculation, diverticula) or demonstrate the obstructive lesion itself (enlarged prostate, posterior urethral valves, cancer of the bladder). If the ureterovesical valves are incompetent, ureteropyelograms will be obtained by reflux.

 

         Retrograde urograms

 

Retrograde urograms may show better detail than the excretory type, but care must be taken not to over distend the passages with too much opaque fluid; small hydronephrosis can be made to look quite large. The degree of ureteral or ureterovesical obstruction can be judged by the degree of delay of drainage of the radiopaque fluid instilled.

 

CT scanning and sonography can also help determine the extent of dilatation and parenchymal atrophy.

         

                                         CT  scanning

 

 

     

                                                 Sonography

 

Isotope scanning. In the presence of obstruction, the radioisotope renogram may show depression of the vascular and secretors phases and a rising rather than a falling excretory phase due to retention of the radiopaque urine in the renal pelvis.

The I activity recorded on the gamma camera will show that the isotope is poorly taken up, slowly transported through the parenchyma, and accumulated in the renal pelvis.

Instrumental examination. Exploration of the urethra with a catheter or other instrument is a valuable diagnostic measure. A stricture or tumor may block passage. Spasm of the external sphincter may make passage difficult. Passage of the catheter immediately after voiding allows estimation of the amount of residual urine in the bladder.

 

                 

 

Residual urine is common in bladder neck obstruction (enlarged prostate), cystocele, and neurogenic (neuropathic) bladder. Residual urine is usually absent with urethral stricture, even though the urinary stream may be markedly impaired.

Measurement of vesical tone by means of cystometry is helpful in diagnosing neurogenic bladder and in differentiating between bladder neck obstruction and vesical atony.

Inspection of the urethra and bladder by means of cystoscopy and panendoscopy may reveal the primary obstructive agent. Catheters may be passed to the renal pelvis and urine specimens obtained. The function of each kidney may be measured and retrograde ureteropyelograms can be made.

 

Interventional uroradiology. If there is doubt about the presence of true obstruction, either the Whitaker test or an isotope renogram can be done. However, Whitaker and Buxton-Thomas (1984) have shown that neither test is without error.

 

 

 

 

 

 

 

 

Differential Diagnosis.

 

 

A thorough examination usually leaves no doubt about the diagnisis. The differential diagnosis under these circumstaces is rarely difficult. If seemingly simple infection does not respond to medical therapy or if infection recurs, obstruction or vesicoureteral reflux is the probable cause, and complete study of the urinary tract is indicated.

Complications.

Stagnation of urine leads to infection, which then may spread throughout the entire urinary system. Once established, infection is difficult and at times impossible to eradicate even after the obstruction has been relieved.

Often the invading organisms are urea-splitting (Proteus, staphylococci), which causes the urine to become alkaline. Calcium salts precipitate and form bladder or kidney stones more easily in aikaline urine.

If both kidneys are affected, the result may be renal insufficiency. Secondary infection increases renal damage.

Pyonephrosis is the end stage of a severely infected and obstructed kidney. The kidney is functionless and filled with thick pus. At times, a plain film of the abdomen may show an air urogram caused by gas liberated by infecting organisms.

Treatment.

Relief of obstruction. Treatment of the main causes of obstruction and stasis (benign prostatic hyperplasia, cancer of the prostate, neurogenic bladder, ureteral stone, posterior ureteral valves, and ureteral stenosis) is described in detail elsewhere in this book.

Lower tract obstruction (distal to the bladder) – With patients, in whom secondary renal or ureterovesical damage (reflux in the latter) is minimal or nonexistent, correction of the obstruction is sufficient. If significant reflux is demonstrated and does not subside spontaneously after relief of obstruction, surgical repair may be needed. Repair becomes imperative if there is considerable hydronephrosis in addition to reflux. Preliminary drainage of the bladder by an indwelling catheter or other means of diversion (e.g., loop ureterostomy) is indicated in order to preserve and improve renal function. If, after a few months of drainage, reflux persists, the incompetent ureterovesical junction should be surgically repaired.

 

                    

 

Upper tract obstruction (above the bladder) – If tortuous, kicked, dilated, or atonic ureters have developed secondary to lower tract obstruction (so that they are themselves obstructive), vesical drainage will not protect the kidneys from further damage; the urine proximal to the obstruction must be diverted by nephrostomy or ureterostomy.

 

 

   Plastic by Alleman   

 

 

 

 Plastic by Anderson-Khinse

 

 

 

 

 

 

   Plastic by Anderson-Khinse

 

 

Plastic by Albaran

 

 

The kidneys then may regain some function. Over a period of many months, the ureter may become less tortuous and less dilated; its obstructive areas may open up. If radiopaque material instilled into the nephrostomy tube passes readily to the bladder, it may be possible to remove the nephrostomy tube. If obstruction or reflux persists, surgical repair is indicated. Permanent urinary diversion (e.g., ureteroileal conduit) may be necessary

If one kidney has been irreversibly damaged, as measured by kidney function tests, urography, sonography, CT scan, or scintigraphy, nephrectomy may be necessary.

Plastic by Culp de Verde

 

Eradication of infection. Once the obstruction is removed, every effort should be made to eradicate infection. If the infection has been severe and prolonged, antibiotics may fail to sterilize the urinary tract.

Operations are plastic and restoring, depending on the reason of hydronephrosis, presence of secondary changes in pelvico-caliceal system. If there is external compression ureterolyse, shift of the vessels or resection of the pelvico-ureteral segment is performed with forming of new pelvico-ureteral anastomosis.

The lateral anastomose of ureter and renal pelvis without resection of the pelvico-ureteral segment is used in case of high coming out of ureter.

Nephrectomy is indicated in case of complete hydronephrotic atrophy.

 

Prognosis

No simple statement can be made about the prognosis in this group of patients. The outcome depends upon the cause, site, degree, and duration of the obstruction. The prognosis is also definitely influenced by complicating infection, particularly if it has been present for a long time.

If renal function is fair to good, if the obstruction or other causes of stasis can be corrected, and if complicating infection can then be eradicated, the prognosis is generally excellent.

 

Ureterohydronephrosis.

Ureterohydronephrosis is the dilation of the ureter, renal pelvis and calyces with gradual renal function failure and parenchymal atrophy. The primary (congenital) hydronephrosis (while construction of the ureter orifice, ureterocele etc) and secondary (acquired) – urolithiasis, traumatic injury, etc are differed. It may be uni- and bilateral.

Clinical findings.

There are 5 stages of the ureterohydronephrosis, owing to pelvic obstruction development:

Hypotonia and dilation of pelvic part of ureter;

Hypotonia of the ureter, its inability for peristalsis, renal excretory dysfunction;

Hypotonia of renal pelvis, calices, ureter, secreting-excretory renal dysfunction;

Hypotonia and evacuative dysfunction of the upper urinary tract;

Atrophy of renal parenchyma.

 

Ureterohydronephrosis may course without any signs. The main signs are ache of various intensity, enlarging of the kidney, microhematuria and leukocyturia when infecting.

Diagnosis is made on the research that is similar to hydronephrosis.

Treatment is surgical. Removal of the obstacle (ureterolyse, ureterolithotomy, suturing of the ureterocele etc), resection of the ureter with anastomosing end-to-end by means of ureterocystoneostomia (direct or non-direct) is performed. Nephrectomy is reasonable in case of atrophy of parenchyma. Prognosis is good if the operative measures are made in time.

 

NEPHROPTOSIS

 

                                                  

Nephroptosis (kidney prolapsus) is the pathological state, at which a kidney is displaced far outside its physiology mobility. Mostly it goes down vertically.

Ethiology and pathogenesis.

A characteristic feature of kidney is mobility of three kinds:

1) Respiratory which is connected with the respiratory motions of thorax and front abdominal wall (their amplitude is from 1,5 to 3-5 sm.);

2) Static, that is shown in transition man from horizontal in the vertical position or vice versa (amplitude 1-2 sm.);

3) Palpation, that is determined by distance, on which it is possible to move (downward and more medial) a kidney at palpation (makes 3-5 sm). If the kidney mobility exceeds mentioned parameters, it is considered pathological (nephroptosis).

In the origin of pathological kidney prolapsus numerous factors of physiologic-anatomical and mechanical, congenital and acquired nature takes part. A leading part in the origin of nephroptosis is taken by the changes of fixing kidney vehicle in combination with action of factors of environment. The fixing kidney vehicle consists of definite anatomic parts: ligaments, vessels, fatty kidney capsule, and kidney fascia. Kidney state depends on the anatomic terms, that are forms and depths of kidney bed, intraperitoneal pressure. To the pathological factors which promote changes of connection kidney vehicle and form circumstances for the development of nephroptosis, belong: contagious diseases that lower mesenchim activity, traumas (high falling, jumps on the legs), unfavorable job conditions (specifically, lasting standing on legs, vibration), rapid losing flash, frequent child birth, decreasing muscle tone of front abdominal wall. Sometimes nephroptosis can be one of the splanchnoptosis manifestations. Nephroptosis exists mainly at women () by age 25-40 years. It is explained by the constitutional features of their organism: a pelvis at women is wider, than at men; paravertabral recesses isn’t so deep, especially from the right side, more opened downward and wider in this place. As a result of pregnancy and births the tone of front abdominal wall sometimes goes down.

At the pathological terms the kidney can considerably go down and take place in the different departments of stomach, in the epigastrical area, in the small pelvis. The right-side nephroptosis exists 5-6 times frequent than the left-side one. It is explained by the lower position of right kidney and stronger connection vehicle of left one. A bilateral prolapsus is marked in 15 % cases of this anomaly. Nephroptosis can be mobile and fixed. Kidney can circle around longitudinal and transversal axis. While circling around longitudinal axis lateral kidney edge becomes a front or even inner, and medial – back or vise versa. While circling around the transversal axis, upper kidney tip lean back and lower moves forward (kidney retrowersio or vise versa). Upper kidney tip can move forward, and lower backward (kidney anteversio).

 

 

 

 

Symtomatology and clinical motion.

 

  Nephroptosis

 

 

Nephroptosis is distinguished to have 4 stages. At 1stage the lower kidney tip can be palpated, II - all kidney is palpated, III - the kidney goes down in pelvis and freely moves in all sides, IV - comes (rotary press) back around the longitudinal or transversal axis.

As far as the prolapsus and rotary press of kidney its vessels stretch and are twisted at the sharp turn of trunk. The diameter of kidney artery diminishes in the 1,5-2 times, and a length is multiplied in the 2-3 times and more. It results in the considerable violation of kidney hemodynamic and urodynamics, lymph drainage from her. The narrowing and tension of artery causes kidney ischemia of bud, and overawing of vain - venous hypertension. The violation of outflow of blood and lymph assists development of pyelonephritis, and at the bilateral pathology – kidney insufficiency. In case of prolapsus kidney is usually mobile and when the body takes horizontal position, kidney takes its usual (physiological) state. It’s a mobile nephroptosis. If around the kidney appears comissures process, it is fixed in pathologic position. Its fixed nephroptosis, which can cause, especially at fixed bend of ureter, spreading calices-pelvis system (pieloectopia, hydronephros), at the violation of urine outlaw from the kidney – stones creation.

In 1 stage kidney prolapsus is not accompanied by the clinical symptoms. With the increase of kidney displacement nephroptosis shows itself with symptom-complex, which is predetermined both by the kidney prolapsus, and by the pathological process, that arises up in her. A sick usually complain of the periodic dull pain in the lumbar area, that increases in case of the physical loading, rapid step, raising heavy things. In the horizontal position of patient the pain disappears.

As far as growth of kidney (that is in II stages of nephroptosis) displacement the pain appears on all stomach, which spreads in the back area. It is a result of tightening of nervous branches of hill’s renalis and its bed. A short, attack pain (kidney colic) can be observed in sick on nephroptosis during the kidney cycling around its limb. Hematuria, erythrocyturia, and proteinuria often accompany a paroxysm of pain.

In III stages of nephroptosis pain becomes permanent, that considerably lowers a capacity of a sick. In 13 % of sick on nephroptosis moderate hypertension, caused by violations of hemodynamic exists also.

The progress of disease results in appearance of new symptoms – kidney colic, hematuria, leukocyturia, pyuria, loss of appetite, headache, promoted fatigability, violation of functions of bowels, periodic rise of body temperature. These symptoms testify to the joining complications - pyelonephritis, hydronephrosis, fornix bleeding, arterial hypertension. Functional kidney state at the 1 and 2 stages of nephroptosis, as a rule, is not changed. At the 3 stage the decreasing of kidneys function is connected with different diseases that complicate nephroptosis.

A diagnostics is based on the complaints of sick, anamnesis data, palpation and roentgenologic research in the horizontal and vertical position of the patients.

 

 

 Ultrasonography

 Ultrasonography

 

        Exretory urography

 

The basic method of examination is IV urography. It allows setting a displacement degree and functional ability of the pathologically mobile kidney. At the kidney turn around axis shade of its bowl on pyelogram is narrow, bowls are shortened. Sometimes bowls are covered by the bowl shade, and then are contours its inexpressive or are not quite determined. At nephroptosis the bends and wrings of ureters are often exposed, wring of, above which an expansion of them and also calices-pelvis system of kidneys is determined.

Radiometry renography and the scanning allow defining the position and function of dropped and contrlateral kidneys.

 

 

                    Kidney arteriography

 

Kidney arteriography, which is executed in the horizontal and vertical position of sick, allows to expose not only displacement of kidney, but also changes of proper kidney artery (length, diameter, corner ofsplitting). In the case of nephroptosis stenosis of kidney artery that exposed in the vertical position of sick disappears in horizontal one. First of all differential diagnostics of nephroptosis carries out with kidney dystonia. In this case see urography in the horizontal and vertical position of sick and aortography is executed. In case of kidney dystopy ureter is shortened, arteries move away from aorta lower than normally.

 

 

n       Renal dystopia variations: 1-pelvic; 2- iliac; 3- lumbar; 4- intrathorathic; 5- normal localization of the kidney.

 

Nephroptosis can be display of splanchnoptosis. For this exposure go to research of digestion organs. In case of differentiation of nephroptosis with tumor, basic diagnostic method there is aortography.

 

Treatment

 

The medical treatment of a patient on nephroptosis can be conservative and surgical. A conservative medical treatment is expedient at 1 stage of disease. It consists of the setting spasmolytic and antiinflammatory medications, carrying a special corset, implementation of complex of physical exercises for the strengthening muscles of front abdominal wall.

 

 

     Fedorov's and Riviera methods

 

 

In case of complication of nephroptosis (often exacerbation chronic pyelonephritis, strong pain, that deprives sick capacity) surgical medical treatment is demanded. It is possible to divide a method of the kidney (nephropexy) fixing on three groups: autoplastic:

Using kidney capsule;

Strengthening of a fascias vagina of kidney;

Fixing by fasciae and by the muscular shred;

Fixing by the skin shred; alloplastic; combinatined (with the removal of occlusion of kidney artery, pyelolythotomy and etc.).

 

       

 

Nephropexia after Riviera in the Pitel-Lopatcin modification

 

At one time the Fedorov and Rivoir methods were widespread.
The most physiological operation of the fixing a dropped kidney there is nephropexia after Rivoir in the Pitel-Lopatcin modification. After lumbotomia and kidney nuking, longitudinal shred of m. psoas on the leg as thick as 1.2-2 sm., as long as 15-20 sm. Its lower tip is pushed into a tunnel under the fibrous capsule of lower kidney part and is fixed by stitches to the capsule. Exactly by this process a new ligament, that holds the kidney in normal position with preservation of its physiological mobility.

 

Fascioplication after the Horash method

 

In the postoperative period a patient is concluded in bed on two weeks with a bit heaved up lower edge.

At children the fascioplication after the Horash method is the effective method of nephropexia. A prognosis in case of timely medical treatment is favorable.

 

Renovascular Hypertension

 

                                         

 

Renovascular disease is one of the most common causes of secondary hypertension. Renovascular hy­pertension is underdiagnosed in clinical practice. Al­though emphasis has been placed on developing ac­curate tests to identify the 5% of hypertensive patients who suffer from renovascular hypertension, there are no perfect screening tests for its detection. Improved detection is possible because of a better understanding of clinical clues and pathophysiology of renovascular hypertension. The diag­nosing of renovascular hypertension is important for several reasons. Renovascular hypertension can be difficult to manage medically. Many renal artery lesions are progressive and may result in com­plete renal artery occlusion despite adequate medical management. Renovascular disease is a major cause of end-stage renal disease, especially in elderly pa­tients.High-renin hypertension is associated with an increased rate of cerebrovascular and cardiovascu­lar complications. Renal revascularization can po­tentially cure or better control the hypertension and reverse renal insufficiency.

Renal parenchymal diseases can also cause hyper­tension In many cases the hypertension is correctable if properly diagnosed and treated.

Etiology

Renal disease in association with hypertension has been recognized since the early nineteenth century. In 1898, Tigerstadt and Bergman demonstrated that a water-soluble substance—extracted from the renal cortex of a healthy rabbit and termed renin—pro­duced marked and sustained hypertension when in­jected intravenously into a second healthy rabbit.

In 1934 Goldblatt described 2 models of experi­mental hypertension. In a 2-kidney animal, clipping of one renal artery results in sustained hypertension. Removal of the clip or of the ischemic kidney returns the blood pressure to normal. This model is analo­gous to unilateral renal artery stenosis in humans: The hypertension is renin-dependent. In humans, as in the Goldblatt 2-kidney, 1-clip model of hyperten­sion, unilateral renal ischemia has been shown to produce high-renin, angiotensin-dependent hyperten­sion that can be cured by reconstruction of the renal artery, percutaneous balloon catheter dilation of the stenosed artery, or nephrectomy. In the second model—1 clip, 1 kidney—the hypertension is sodium volume-dependent. Blockade of the renin-angiotensin system has little effect on blood pressure, unless the animal is sodium-depleted. This model is analogous to renal artery stenosis in a solitary kid­ney. It may also resemble bilateral renal artery steno­sis.

Natural History

Atheromatous renal arterial disease predominantly occurs in the proximal third of the renal artery and is often part of diffuse atherosclerosis, affecting many other vascular beds (eg, coronary, carotid, and pudendal arteries). In many cases, a plaque in the wall of the aorta may encroach on the ostium of the renal artery. Atheromatous disease of the renal artery most commonly afflicts older men. The disease is often bi­lateral (40%) and progressive (44%), resulting in to­tal occlusion (16%) despite medical treatment of the hypertension.

 

 

Fibromuscular dysplasia of the renal arteries is the most common cause of renovascular hypertension in younger patients. It is diagnosed in one-third of pa­tients with renovascular hypertension. These lesions can be progressive in up to 33% of cases but rarely result in total arterial occlusion. There are 4 different pathologic types of fibromuscular dysplasia. Medial fibroplasia is the most common and accounts for 70% of cases. The angiographic appearance is that of a string of beads owing to thickening of the media in­terspersed with areas of aneurysmal dilation. These lesions are rare in children.

In a study of potential renal donors, 27% of the normotensive patients with incidentally found fibro­muscular dysplasia subsequently became hyperten­sive over the ensuing 7.5 years.

Thus, renal arterial lesions are often progressive. This fact provides strong support for angioplasty or surgical revascularization to maintain renal function and correct hypertension.

Pathogenesis

                                     

The renin-angiotensin-aldosterone system is an integrated hormonal cascade that simulta­neously controls blood pressure and sodium and potassium balance, and influences regional blood flow. Renin is a proteolytic enzyme produced in the juxtaglomerular cells of the afferent arterioles. It acts on renin substrate (angiotensinogen), an alpha-2 globulin produced in the liver, to form the decapeptide angiotensin I. Converting enzyme cleaves 2 amino acids from angiotensin I to form the octapep-tide angiotensin II, a potent arterial vasoconstrictor. Angiotensin II also stimulates the zona glomerulosa of the adrenal gland to secrete aldosterone. Elevation of blood pressure and restoration of sodium balance inhibit further renin secretion.

The mechanisms responsible for renin secretion in­clude an afferent arteriolar baroreceptor responding to decreased renal perfusion pressure, a sensor at the macula densa responding to decreased delivery of so­dium and chloride to the distal tubule, and increased activity of the sympathetic nervous system, mediated by beta-1 -adrenergic receptors. Frequent causes of hypersecretion of renin include sodium depletion, hem­orrhage, shock, congestive heart failure, and renal artery stenosis.

Plasma renin activity is closely related to the pa­tient's sodium intake and urinary sodium excretion, ie, sodium balance. The renin-angiotensin-aldosterone system is activated in response to sodium restriction and suppressed by sodium loading. Plasma renin activ­ity must therefore be correlated with the sodium bal­ance in order to be meaningful.

The renin angiotensin system is undoubtedly the main mechanism responsible for renovascular hyper­tension. However, other mechanisms appear to play a causative role. There is evidence that activity of the

sympathetic nervous system may be increased. Two-kidney, 1-clip rats have a high rate of norepinephrine release. Sympathetic blockade with chlorisondamine reduces both norepinephrine levels and blood pres­sure. Nitrous oxide appears to play a role as well. Feeding a nitric oxide inhibitor to dogs exacerbated the hypertension produced by clipping one of 2 healthy kidneys. It is believed that nitric oxide may counter the vasoconstrictor effects of angiotensin.

Pathology

Stenosis of the renal artery (and, therefore, reno­vascular hypertension) is most commonly caused by arteriosclerotic plaques or fibromuscular dysplasia. Not all renal artery stenoses are physi­ologically significant and cause hypertension, how­ever. A lesion must produce a reduction in luminal diameter of at least 70% before renal plasma flow is reduced to the point that clinically significant ischemia results. The clinical significance of an ana­tomic stenosis noted on angiography is assessed by renin assays, as discussed subsequently.

Other urologic lesions that may cause renin-depen-dent hypertension include obstructive uropathy, be­nign and malignant renal masses, and chronic pye­lonephritis, the latter most commonly associated with vesicoureteral reflux. In some patients, elevated levels of plasma renin activity return to nor­mal, and hypertension is alleviated after appropriate surgical treatment of the underlying urologic disorder. However, hypertension due to renal parenchymal dis­ease usually is not curable by surgical means. Most pa­tients require medical management to control blood pressure.

History & Physical Examination

A.                          History: A complete and thorough medicalhistory and physical examination provide important information about the patient's current general health, past medical history, and family medical history.

Clinical clues suggestive of renovascular hypertension.

 

Clues from history

Comment

Hypertension in the absence of any family history of hypertensive disease

Suspect renovascular hypertension if the family history is negative; however, about one-third of patients with renovascular hypertension have a positive family history.

Age of onset of hypertension is under 25 years or over 45 years

Average age of onset of essential hypertension is 31 ±10 (SD) years. Children and young adults usually have fibromuscular disease, whereas adults over age 45 years are more likely to have atherosclerotic narrowing of the arteries.

Abrupt onset of moderate to severe hypertension

Essential hypertension usually begins with a labile phase before mild hypertension becomes established, whereas the natural history in renovascular hypertension is usually more compressed, with the disease often appearing initially as moderate hypertension of recent onset.

Development of severe or malignant hypertension

Renovascular hypertension often becomes moderately severe and may cause accelerated or malignant hypertension; both forms of hypertension involve markedly increased secretion of renin.

Headaches

Essential hypertension is usually asymptomatic; headaches occur more commonly with renovascular hypertension and may be related to its greater severity or the high levels of angiotensin II (a potent cerebrovascular vasoconstrictor) associated with this disease.

Cigarette smoking

A recent survey showed that 74% of patients with fibromuscular renal artery stenosis are smokers; 88% of those with atherosclerotic disease smoke.

White race

Renovascular hypertension is uncommon in blacks.

Resistance to or escape from adequate control of blood pressure with standard diuretic or antiadrenergic therapy

Renovascular hypertension typically responds poorly to diuretics and ofen responds only transiently to antiadrenergic drugs.

Excellent antihypertensive response to converting enzyme inhibitors, eg, captopril

Converting-enzyme inhibitors block the renin-angiotensin-aldosterone system most effectively and are highly specific agents.

Clues from physical examination and routine laboratory studies

Retinopathy

Hemorrhage, exudates, or papilledema indicates accelerated or malignant hyper­tension.

Abdominal or flank bruit

Bruits are not pathognomonic of renovascular hypertension, since they are common in elderly persons and occasionally occur in younger patients who have no apparent vascular stenosis.

Carotid bruits or other evidence of large-vessel disease

Vascular pathologic processes are not limited to the renal bed.

Hypokalemia exists in the untreated state or persists even after administra­tion of a thiazide diuretic

Increased aldosterone secretion by the renin-angiotensin-aldosterone system reduces serum potassium level. This does not occur in untreated essential hyper­tension. Thiazide diuretics accentuate this phenomenon in renovascular hyper­tension.

 

The patient's age and circumstances at onset of hypertension, recorded blood pressure ranges, previous treatment, results of therapy, and history of end-organ damage are noted. The past history is investigated for evidence of diseases (eg, glomerulonephritis, chronic pyelo­nephritis with or without vesicoureteral reflux, hydronephrosis, urolithiasis) or other factors (eg, renal trauma, radiation therapy to the abdomen) that could contribute to the development of hypertension.

Hypertension may have an abrupt onset and progress rapidly in children with Wilms tumor, in young adults with fibromuscular dysplasia, and in older patients with arteriosclerotic occlusion of therenal artery. Anorexia, weight loss, and malaise may be signs of malignant disease leading to elevated blood pressure. However, the absence of symptoms is not sufficient to rule out a diagnosis of curable hy­pertension.

Pulmonary edema is relatively frequent in patients with advanced renovascular hypertension with bilat­eral disease and azotemia.

 

B. Physical Examination: Physical exam­ination should include serial measurements of the pa­tient's blood pressure to establish the degree of hyper­tension. Measurements are taken in each arm with an appropriate-sized cuff while the patient is standing, sitting, and lying down. If 3 measurements are higher than 140/90 mm Hg in an adult, further evaluation is warranted. A funduscopic examination should be per­formed to look for hemorrhage, exudates and pa-pilledema. The physician should palpate all peripheral pulses. Diminution of pulses and decreased blood pressure in the lower extremities in a young patient may signify coarctation of the aorta; an intrascapular murmur is another characteristic sign. In patients with renal artery stenosis, a continuous abdominal bruit may be heard on either side of the midline immediately above the umbilicus.

Laboratory Evaluation

A. Renovascular Hypertension: The low prevalence of renovascular hypertension among hy­pertensive patients, together with the cost and less than perfect accuracy of screening tests for renovas­cular hypertension, makes screening for this disease impractical. Pickering and colleagues have suggested that for patients with a low index of suspected dis­ease, only basic evaluation is needed (see below). These include patients with borderline, mild, or mod­erate hypertension in the absence of clinical clues, and patients with low renin hyperten­sion. For patients with a moderate index of suspected disease, noninvasive tests should be performed as de­scribed below. For this group the prevalence of reno­vascular hypertension is between 5% and 15%. For these patients, the predictive value of a negative re­sult of a diagnostic test with a sensitivity and speci­ficity of 90% would exceed 98%. The predictive value of a positive test would be 32%, which would justify arteriography.

For patients with a high index of suspected dis­ease, eg, those with severe hypertension (diastolic > 120 mm Hg) refractory to aggressive medical treat­ment or with an increase in creatinine, or patients with malignant hypertension (type III or IV retinopa-thy), arteriography is justified even if the noninva­sive diagnostic tests are negative or inconclusive. These patients are likely to suffer deterioration in re­nal function when treated with converting-enzyme inhibitors and are at high risk for ischemic nephropa-thy.

1. Basic tests-Laboratory examination of pa­tients with suspected renovascular hypertension should begin with basic tests that assess the patient's general health: complete blood count, serum electrolytes and fasting blood glucose determi­nations, blood urea nitrogen and serum creatinine measurements, urinalysis and urine culture, and an electrocardiogram.

2. Plasma renin activity profile-In patients in whom the diagnosis of hypertension has been defini­tively established, evaluation with a plasma renin ac­tivity profile (plasma renin activity must be plotted against 24-h urinary sodium excretion) is performed. These measurements should be obtained while the patient is on a diet containing normal amounts of sodium; antihypertensive medication must be with­held for 2 weeks before sampling. The blood sample for the renin determination is drawn at the end of the 24-h period in which the urine is collected and after 4 h of ambulatory activity. This test will reveal ele­vated plasma renin activity levels in about 80% of patients with renovascular hypertension (Figure 45-6, left). However, 15% of patients with essential hypertension also have high renin, which lowers the predictive value of the test.

3. Captopril challenge test-Peripheral plasma renin activity is measured before and 1 h after admin­istration of captopril (a converting-enzyme inhibitor), 25 mg orally. In renin-dependent hypertension, inhi­bition of the converting enzyme occurs. If the 3 crite­ria found by Muller are present in a pa­tient with normal renal function who is not taking diuretics, renovascular hypertension can be distin­guished from essential hypertension. Other investigators confirmed the value of the captopril test, al­though they found it less reliable than first reported. The overall sensitivity is approximately 61%, and specificity is 86%. Differences in the reported accu­racy of the test may be attributed to a number of fac­tors. The assay used, the patient selection, and posi­tion during testing can all alter outcomes. Previous sodium depletion due to use of diuretics, dietary re­strictions, and chronic treatment with captopril in­creases plasma renin activity and causes the captopril challenge test to be nonspecific. Patients taking beta blockers remain responsive to the test as described previously, unless the baseline plasma renin activity is less than 2.5 ng/mL/h, in which case the test may be unreliable.

Most studies have found the test to be less reliable in azotemic patients, and it does not discriminate between unilateral and bilateral disease. Moreover, the test may be less reliable in black patients than in white patients.

4. Captopril renography-A recently intro­duced addition to the captopril test is the compari­son of both 131I-hippurate and 99mTc-diethylenetri-aminepentaacetic acid (99mTc-DTPA) renography before and after single-dose captopril. Patients with renal artery stenosis show a fall in glomerular filtra­tion confined to the affected kidney and thus a selec­tive fall in 99mTc-DTPA uptake with preservation or even an increase in 131I-hippurate and 99mTc-DTPA uptake to the normal side. Captopril renography has been found to have 90-92% sensitivity and 86-93% I sensitivity in various studies. It has become one of the most popular noninvasive tests for renovascular hypertension. Captopril renography may be less reliable in patients with impaired renal function or in pa­tients with severe renal artery stenosis.

5. Renal vein renin sampling-Patients with high peripheral plasma renin activity levels or those in whom the captopril challenge test is positive may undergo further evaluation with renal vein sampling for renin. Samples are collected from each renal vein (VI and V2) and from the distal inferior vena cava before and after administration of captopril, 25 mg orally.

According to criteria established by Vaughan et al (1973), potentially reversible hypertension is charac­terized by ipsilateral hypersecretion of renin ([VI -A] divided by A < 0.50), contralateral suppression of renin secretion ([V2 - A] divided by A = 0), and an increase in the peripheral plasma renin activity level. In patients with stenoses of both renal arteries, the pattern of renal vein renins often shows the same degree of asymmetry as in unilateral steno­sis, lateralizing to the kidney with the greater degree of stenosis. The most marked asymmetry is seen in patients who have complete occlusion of one renal artery.

Renal vein renins are performed less widely today, in part because of high cost, but also owing to the high false-negative rate that tends to exclude patients from the benefit of renal revascularization.

6. Ultrasound scans-Renal Doppler ultra­sound scanning is gaining widespread use for the evaluation of renovascular disease.

 

 

  Doppler ultra­sound scanning

 

 

Doppler ultra­sound scanning can record velocity profiles of blood flow from the renal arteries and parenchyma. A number of criteria have been used to identify a stenosis. One is to take the ratio of the peak systolic velocity between the aorta and the renal artery. A renal-aortic ratio of 3.5 or more and peak systolic velocity of more than 200 cm/s are considered in­dicative of a significant stenosis. Another is the "tardus-parvus" pattern, which occurs distal to a stenosis and is characterized by a smaller and more rounded waveform.

Doppler exam of the main renal arteries may fail technically in up to 40% of patients. An alternative strategy is to use the flow profile from the interlobar arteries. This can be quantified as the renal resistive in­dex, which is defined as the peak systolic flow velocity - peak end-diastolic flow velocity/peak systolic flow velocity x 100. A difference of resistive index be­tween the 2 kidneys of more than 5% has been used as an indication of renal artery stenosis. Also, the absence of flow in the artery and a low-amplitude parenchymal signal is diagnostic of occlusion of the renal artery. In a meta-analysis of the cost-effectiveness of different methods for diagnosing renovascular hypertension, Blaufox et al (1996) concluded that the sensitivity of

Doppler testing was no better than captopril renography and that, although the specificity was higher, this was offset by the high technical failure rate of 17%.

The advantages of duplex scanning are that it is noninvasive and free of adverse effects. For the pa­tient with an elevated serum creatinine in whom the physician wants to determine, with a high degree of likelihood, whether significant renal artery disease is contributing to the azotemia, duplex scanning is use­ful. It can also be used for following up patients after percutaneous transluminal renal angioplasty, renal artery stents, or bypass surgery.

An interesting new development has been to use the hemodynamic effects of captopril to improve the diagnostic accuracy of Doppler scanning. Rene et al (1995) found that the pulsus tardus pattern was more likely to be seen after captopril in stenotic renal arter­ies; 68% of stenoses could be diagnosed before cap­topril, and 100% could be diagnosed after captopril. Another technique is to compare the resistive index of the ischemic and nonischemic kidneys before and after captopril.

7. Magnetic resonance angiography (MRA)-Magnetic resonance angiography is a new technique that has the ability to visualize arteries noninvasively without contrast.

    

 

 

 Using phase contrast imaging, the gadolinium-enhanced MRA with 3-dimensional re­construction of the images, sensitivities and specifici­ties have been reported to be > 90% when compared with conventional angiography. Magnetic resonance angiography is much better at detecting proximal than peripheral lesions. The low false-negative rate for detecting major atherosclerotic lesions means that a normal MRA obviates the need for traditional an­giography in high-risk patients. Its expense and the high degree of expertise required to obtain and cor­rectly interpret good images precludes its use as a general screening test.

8. Helical (spiral) computed tomography-Computed tomography (CT) can be used to visualize arteries as well as solid tissues.

 

 

 

Spiral CT differs from conventional CT in that it incorporates a rapidly rotating gantry, which enables acquisition of images with sufficient rapidity to visualize arteries as the contrast passes through. The resolution compares very favorably with that of MRA, although both techniques have limited ability to detect accessory re­nal arteries. The main appeal of spiral CT is that it enables construction of 3-dimensional images of the aorta, renal arteries, and kidneys all at the same time, using one of 2 procedures (maximal intensity projec­tion or surface shaded display). Both are time-con­suming to construct and require a highly skilled radi­ologist or technician. The sensitivity and specificity of spiral CT for detecting renal artery stenoses have been reported to be in the region of 95%. Unlike MRA, it can be used to examine the patency of renal arteries with intravascular stents. The chief disadvan­tages are the cost and the much greater volume of contrast agents needed to obtain adequate images (about 150 mL, compared with 15 mL for conven­tional digital subtraction angiography). This greatly limits its use in patients with impaired renal function.

9. Other tests- Excretory urography is not gener­ally recommended as an initial screening test for reno-vascular hypertension because it has a sensitivity of only 75% and a specificity of 86% (Harvey et al, 1985). It is nonetheless useful in patients with a history of verified or suspected urologic disease and in the lo­calization of anatomic defects before surgery.

 

 

 

                   

 

 

 

                   

 

Arteriography or digital intravenous subtraction angiography has not greatly in­creased the predictive value of screening tests for identifying renovascular hypertension. These methods involve intravenous injection of con­trast material to delineate the anatomy of the renal ar­teries and urinary tract. However, arteriographic or angiographic demonstration of an arterial lesion must be supplemented by evidence of abnormal levels of renin secretion to prove that unilateral ischemia is the cause of renovascular hypertension.

 

B. Renal Parenchymal Disease: In patients with suspected renal parenchymal disease, preoperative evaluation of plasma renin activity is similar to that described for patients with renovascular hyper­tension. The captopril challenge test is recommended in these patients to elicit evidence of a reactive rise in plasma renin activity and a fall in blood pressure. Hypertension due to renal parenchymal disease is less frequently curable by surgical treatment than is renovascular hypertension. Nephrectomy should be avoided if the blood pressure can be controlled with antihypertensive medication and if the glomerular fil­tration rate in the involved kidney is sufficient to en­sure the patient's survival if removal of the contralat-eral kidney ever becomes necessary.

 

Treatment

Patients with known or suspected hypertension must be methodically evaluated to identify those with renin-dependent hypertension and to plan individual­ized treatment.

There are 3 principal modes of treatment for reno­vascular hypertension: medical, surgical, and angioplasty with and without stents. Because renal artery stenoses impair renal function and cause hyperten­sion, renal revascularization is preferred over med­ical management.

 

A. Medical Measures: Medical management of patients was difficult before the advent of modern anti-hypertensive therapy, and survival has improved with surgical treatment. Currently, blood pressure can be controlled effectively but renal function may de­teriorate, especially in patients with atherosclerotic disease. Converting-enzyme inhibitors are the most powerful drugs for patients with renovascular hyper­tension. However, the inhibition of angiotensin II con­striction of the efferent glomerular arteriole may lead to decreased glomerular filtration rate and even renal failure in patients with bilateral renal arterial disease. In patients with bilateral renal artery stenosis or steno­sis of a renal artery in a solitary kidney, use of convert­ing-enzyme inhibitors may increase creatinine and blood urea nitrogen. Moreover, renal artery stenosis is progressive, with 15% of patients suffering complete occlusion despite adequate blood pressure control. Angiotensin receptor blockers are being used to treat renovascular hypertension. As yet the clinical data as to the effectiveness of these medications are limited. Calcium channel blockers vasodilate the afferent arte­riole and have been shown to lower blood pressure with less impairment of function than converting en­zyme inhibitors. In summary, medical management is limited to patients who are not candidates for interven­tion or in whom revascularization has failed. In these patients both blood pressure and renal function must be monitored carefully.

B. Transluminal Angioplasty:       

 

 

Patients who meet the criteria for reversible renovascular hyper­tension can now be treated with percutaneous transluminal balloon dilation of the stenotic renal artery. In success­ful cases, angiograms obtained after transluminal an­gioplasty show enlargement of the diameter of the re­nal artery, and measurements show that the renin activity returns to normal levels and the blood pressure likewise returns to normal or near-normal levels. Angioplasty is now the initial treatment of choice in all patients with fibromuscular hyperplasia and in patients with atherosclerotic disease, excluding those with osteal lesions and total occlusion.

 

 

 

 

Successful dilation in more than 80% of these patients precludes the need for major surgery and can lower blood pressure while preserving or improving renal function. The results in patients with fibromuscular dysplasia are good. There is an overall benefit of 93% (58% cured, 35% improved, and 7% failed). Restenosis is uncommon in these patients. In patients with renal artery stenosis due to atheroma, the benefit is about 80% (22% cured, 58% improved, and 20% failed). The restenosis in patients with atheromatous disease is 19% after 9 months. It has been shown that failed angioplasty does not reduce the success rate of subsequent surgi­cal renal revascularization.

 

 

 

 

 

 

 

 

 

 

C. Renal Artery Stents: Renal artery stents can be placed to maintain patency of the renal artery following angioplasty. The indications for stent placement include renal ostial stenoses that have a high restenosis rate following angioplasty. Other atheromatous lesions that were dilated unsuccessfully or have restenosed can be stented as well. The restenosis rate for these high-risk patients is less than that for angioplasty alone.

D. Surgical Measures: Surgery is indicated for patients with total renal artery occlusion and preserva­tion of function, osteal lesions, and complex lesions, and those in whom percutaneous transluminal dilation is not successful. The first surgical cure of hyper­tension was achieved by unilateral nephrectomy. However, unilateral nephrectomy has benefited only 26-37% of the large group of unselected patients with hypertension who have been so treated. Unilateral nephrectomy is now reserved for treatment of 2 groups of patients with hypertension: (1) those who have poor or absent renal function in the involved kidney but nor­mal function in the contralateral kidney and in whom attempts at revascularization have failed, and (2) those at such high risk that the loss of functioning nephrons is offset by the elimination of the cause of significant excess renin secretion. Partial nephrectomy may be performed if the kidney has multiple renal arteries and only one is stenotic.

 

 

                         

 

Today, surgical treatment emphasizes preservation of renal function. Accordingly, various methods may be used to attempt to revascularize an ischemic kid­ney; these include endarterectomy, aortorenal bypass graft using the saphenous vein or hypogastric artery, and hepatorenal and splenorenal bypass procedures for patients with severely diseased aortas. Hyperten­sion has been cured or improved in more than 90% of the carefully selected patients treated surgically by experienced operating teams; the mortality rate has been about 2%. More favorable results have been achieved in patients with fibromuscular disease, who tend to be younger and healthier than the patients presenting with atheromatous disease. Renal revascu­larization for preservation of renal function in azotemic patients with renal arterial disease is gain­ing wider acceptance irrespective of blood pressure or renin values. All azotemic patients without a clear cause of renal failure should be evaluated for renal arterial

 

References:

a) basic literature:

1. Donald R. Smith, M.D. General Urology, 11-th edition, 1984, p.149-162, 598-608

2. Official Journal of the European Association of Urology /2002-2007/.

3. Urological Guidelines (European Assosiation of Urology) Health Care Office /august 2004 edition/.

4. Urology edited by N.A.Lopatkin, Moscow, 1982, p.146-152, 282-292, 363-378

 

b) supplementary literature:

1. European Urology Supplements /2002-2007/.

2. European Urology via www.eropeanurology.com

3. Urology The Gold Jounal /www.goldjournal/net/.

4. Scientific Foundations of Urology. Third Edition 1990. Edited by Geoffrey D. Chisholm and William R. Fair, MD. Heinemann Medical Books, Oxford.,p.107-123