Medicine

Lesson 2

Lesson 2                                  

ACUTE PYELONEPHRITIS

 

Etiology

Acute pyelonephritis is an infectious inflamma­tory disease that involves both the parenchyma and the pelvis of the kidney; it may affect one or, on occasion, both kidneys.

Aerobic gram-negative bacteria are the principal causative agents; common strains of E coli are the predominant pathogens. All species of Proteus are especially important because they are potent producers of urease, an enzyme that splits urea and produces highly alkaline urine that favors the precipitation of phosphates to form magnesium ammonium phosphate (struvite) and calcium phosphate (apatite) stones. Klebsiella species are less potent producers of urease but elaborate other substances that favor urinary stone formation.

Gram-positive bacteria other than the enterococ-cus Streptococcus faecalis seldom cause pyelone­phritis. Staphylococci may infect the kidney by the hematogenous route and cause bacteriuria and renal abscesses. Obligate anaerobic bacteria rarely cause pyelonephritis.

 

Pathogenesis

Renal infection usually ascends from the urethra and lower genitourinary tract. Hematogenous infec­tion of the kidney occurs infrequently; lymphatic spread occurs rarely, if ever.   

                                     

 

Microbial      organism

Acute uncomplicated cystitis (%)*

Acute
uncomplicated pyelonephritis (%)

Complicated
UTI(%)

Catheter-associated UTI (%)

Escherichia coli

68

89

32

24

Staphylococcus saprophyticus

8

0

1

0

Proteus

6

4

4

6

Klebsiella

4

4

5

8

Enterococci

3

0

22

7

Pseudomonas

0

0

20

9

Mixed

3

5

10

11

Yeast

0

0

15

8

 

 

 

The short urethra in girls and women and its close proximity to the anus allow periurethral pathogenic bacteria easy access to the bladder during sexual inter­course or urethral manipulation. Girls and women with breached local defenses due to biologic, anatomic, or other abnormalities frequently experience introital and periurethral colonization by pathogenic enteric bac­teria and are especially prone to infection that ascends from the urethra.

Males are less susceptible to ascending urethral infection because the male urethra is much longer than the female urethra and the meatus is not so near the anus and because the prostate normally secretes an­tibacterial factors that give some protection against invading pathogens.

Once pathogenic bacteria reach the bladder via the urethra, whether infection becomes established is influenced by the quality of the bladder defenses: the efficacy of voiding and muscle coordination, the anti­microbial properties of the urine, and factors that allow or inhibit bacterial adherence to surface cells.

Once bladder infection is established, whether infection ascends via the ureters and involves the kid­neys is influenced by microbial virulence factors, the presence or absence of vesicoureteral reflux, the qual­ity of ureteral peristalsis, and the susceptibility of the renal medulla to infection.

 

 

    Infection goes at the ureter from the bladder because of the        vesicoureteral reflux.

 

 

 

                        The secondary pyelonephritis goes with urostasis

 

 

 

 

 

Causes

Common causes

Ascending UTI: 75% of pyelonephritis cases are due to E. coli; 10% to 15% are caused by other Gram-negative rods, Klebsiella, Proteus, Enterobacter; others include Pseudomonas, Serratia, and Citrobacter. Gram-positive agents include Enterococcus faecalis and, less commonly, Staphylococcus aureus anaerobes

Fungal agents, especially Candida spp., are seen in immunocompromised patients and patients with diabetes

Rare causes

Other infecting organisms may include Salmonella, Leptospira, Mycoplasma, Chlamydia

In travelers, the possibility of tropical infection and Echinococcus should be kept in mind

Contributory or predisposing factors

Diseases or conditions that cause stasis of urine in the urinary tract promote multiplication of organisms in the urinary tract and ascension of infection

Diseases that impair immunity promote multiplication of organisms in the urinary tract and ascension of infection

Presence of a device in the urinary tract promotes multiplication of organisms in the urinary tract and ascension of infection

 

Obstructions to urine flow:

Vesicoureteric reflux (VUR) is the most important predisposing factor in children younger than 6 years

Obstruction of outflow of bladder: benign prostatic hypertrophy, prostatic carcinoma, bladder tumors

Carcinoma arising from renal tract, for example, renal cell carcinoma, bladder cancer, ureteric tumors; carcinoma arising outside renal tract and impinging on it, for example, bowel, cervix, prostate

Radiotherapy or surgical damage to ureters

Pregnancy encourages reflux by dilatation of the ureters and probably reduces immunity of renal parenchyma

Calculi cause obstruction and stasis, and act as foci for infection

Neurologic abnormalities, for example, spina bifida, multiple sclerosis

Polycystic kidney disease, affects 0.8/1000 of the population and is inherited as an autosomal dominant trait

Renal parenchymal damage due to tuberculosis

Neurogenic bladder following trauma or secondary to neurologic disorders such as diabetic neuropathy

 

Impaired immunity:

HIV

Myeloproliferative disorders

Diabetes

Organ transplantation (transplant pyelonephritis of the new kidney)

Chemotherapy

Stasis and impaired immunity may coexist in patients with:

Malignancy, especially after chemotherapy

Diabetes

Devices in the urinary tract:

Indwelling bladder catheters (Foley catheters)

Ureteral stents

 

Classification

*    The primary and secondary pyelonephritis are distinguished.

*    There is  no dysfunction of the  urine  outflow during the primary pyelonephritis.

*    The secondary pyelonephritis goes with urostasis.

 

*    1/ The unilateral and bilateral.

*     a/ Acute /purulent, serous/

*     b/ Chronic;

*     c/ Relapsing course.

*    2/ By the mode of bacteria pathway there are differed                             

*    3/ a/ hematogenous /ascending/;

*    b/ urogenic /ascending/;

*    c/ urolithiasis /infected urinary stones/;

*    d/ tuberculosis of the kidneys;                                                                  

*    e/ the other renal diseases.

*    By the course, age, stage of the organism there are differed:

*    1/ the pyelonephritis of newborn;

*    2/ the pyelonephritis of the aged patients;

*    3/ the pyelonephritis of the pregnant women;

*    4/ the pyelonephritis in diabetes mellitus patients.

*    The acute pyelonephritis may be complicated with purulent nephritis, carbuncle of the kidney, the renal abscess, renal insufficiency.

 

 

Clinical Findings

A. Symptoms Symptoms

Back pain orflank pain

Chills with shaking

Severe abdominal pain (occurs occasionally)

Fatigue

Fever

Higher than 102 degrees Fahrenheit

Persists for more than 2 days

General ill feeling

Chills with shaking

Mental changes or confusion*

 Skin changes

Flushed or reddened skin

Moist skin (diaphoresis)

Warm skin

 Urination problems

Blood in the urine

Cloudy or abnormal urine color

Foul or strong urine odor

Increased urinary frequency or urgency

Need to urinate at night (nocturia)

Painful urination

Vomiting, nausea

 

*    Mental changes or confusion may be the only signs of a urinary tract infection in the elderly

 

 

B. Signs: The classic presentation in patients with acute pyelonephritis is as follows:

 

Fever - This is not always present, but when it is, it is not unusual for the temperature to exceed 103°F (39.4°C)

 

Costovertebral angle pain - Pain may be mild, moderate, or severe; flank or costovertebral angle tenderness is most commonly unilateral over the involved kidney, although bilateral discomfort may be present

 

Nausea and/or vomiting - These vary in frequency and intensity, from absent to severe; anorexia is common in patients with acute pyelonephritis

 

Gross hematuria (hemorrhagic cystitis), unusual in males with pyelonephritis, occurs in 30-40% of females, most often young women, with the disorder.

 

Symptoms of acute pyelonephritis usually develop over hours or over the course of a day but may not occur at the same time. If the patient is male, elderly, or a child or has had symptoms for more than 7 days, the infection should be considered complicated until proven otherwise.

 

The classic manifestations of acute pyelonephritis observed in adults are often absent in children, particularly neonates and infants. In children aged 2 years or younger, the most common signs and symptoms of urinary tract infection (UTI) are as follows:

 

Failure to thrive

 

Feeding difficulty

 

Fever

 

Vomiting

 

Elderly patients may present with typical manifestations of pyelonephritis, or they may experience the following:

 

Fever

 

Mental status change

 

Decompensation in another organ system

 

Generalized deterioration

 

 

C. Laboratory Findings: The hemogram typi­cally shows significant leukocytosis (polymorphonu-clear neutrophils and band cells); the erythrocyte sedimentation rate is increased. Urinalysis usually shows cloudy fluid with heavy pyuria, bacteriuria, mild proteinuria, and often microscopic or gross hematuria. Leukocyte casts and glitter cells (large polymorphonuclear neutrophils containing cytoplas-mic particles that exhibit dramatic brownian move­ment) are occasionally seen. Quantitative urine culture generally grows the responsible pathogen in heavy density (≥100,000 colonies/mL); sensitivity tests are helpful in therapy and of vital importance in the man­agement of complicating bacteremia. Serial blood cul­tures are indicated, because bacteremia commonly ac­companies acute pyelonephritis. In uncomplicated acute pyelonephritis, total renal function generally re­mains normal, and the serum creatinine level is not elevated.

 

 

Diagnosis

 

In the outpatient setting, pyelonephritis is usually suggested by a patient’s history and physical examination and supported by urinalysis results. Urine specimens can be collected through the following methods:

 

Clean catch

Urethral catheterization

Suprapubic needle aspiration

Urinalysis can include the following:

Dipstick leukocyte esterase test (LET) - Helps to screen for pyuria

Nitrite production test (NPT) - To screen for bacteriuria

Examination for hematuria (gross and microscopic) and proteinuria

 

Urine culture is indicated in any patient with pyelonephritis, whether treated in an inpatient or outpatient setting, because of the possibility of antibiotic resistance.

 

Imaging studies that may be used in assessing acute pyelonephritis include the following:

 

Computed tomography (CT) scanning - To identify alterations in renal parenchymal perfusion; alterations in contrast excretion, perinephric fluid, and nonrenal disease; gas-forming infections; hemorrhage; inflammatory masses; and obstruction

 

Magnetic resonance imaging (MRI) – To detect renal infection or masses and urinary obstruction, as well as to evaluate renal vasculature

 

Ultrasonography - To screen for urinary obstruction in children admitted for febrile illnesses and to examine patients for renal abscesses, acute focal bacterial nephritis, and stones (in xanthogranulomatous pyelonephritis)

 

Scintigraphy - To detect focal renal abnormalities

 

CT and MR urography - Used in the evaluation of hematuria

 

X-Ray Findings:

 

                  Plain film

 

 A plain film of the abdomen may show some degree of obliteration of the renal outline owing to edema of the kidney and perinephric fat. Suspicious calcifications, must be carefully evaluated, because infected renal stones and calculous obstruction complicating pyelonephritis require spe­cial management.

           Excretory urograms

 

Excretory urograms performed during the acute stage of uncomplicated pyelonephritis usually show few abnormalities but are important in surveying for possible complicating factors. The severely infected kidney may appear enlarged, show a decreased nephrogram effect on the initial film, and reveal little or no caliceal radiopaque material. Following appropriate therapy, the urograms return to normal.

Voiding cystograms are best delayed until several weeks after the infection is cleared; otherwise, tran­sient vesicoureteral reflux, often associated with the accompanying cystitis, may be confused with more serious permanent reflux.

 

Retrograde cystogram (vesicoureteral reflux)

E. Radionuclide Imaging: At times, imaging ' the kidneys with gallium-67 helps to determine the site of infection and distinguish between acute pyelone­phritis and renal abscess. Despite some false-positive and false-negative images, Hurwitz et al (1976) claim 86% accuracy in confirming acute pyelonephritis by this method.

 

Instrumental Examination

 

                 

 

*    There can be seen the bullous edema of the urethral orifice because of calculus at the intravesical portion, ureterocele, tumor compression.

*    Chromocystoscopia shows the range even sometimes the cause of the functional loss of the urine outflow.

 

 

                                                                                           Differential Diagnosis

Differential Diagnosis

Because of the location and nature of the pain, pancreatitis at times may be confused with acute py­elonephritis. Elevated serum amylase and normal re­sults of urinalysis help to confirm a diagnosis of pan­creatitis and rule out pyelonephritis.

Basal pneumonia is a febrile illness that causes pain in the subcostal area. The pleuritic nature of the pain and the chest x-ray usually allow differentiation.

Acute intraabdominal disease, including such conditions as acute appendicitis, cholecystitis, and di-verticulitis, must at times be distinguished from acute pyelonephritis. Although the signs and symptoms may be confusing initially, the normal urinalysis associated with primary gastrointestinal disease and other laboratory tests should make the differential diagnosis un­complicated.

In women, the onset of acute pelvic inflammatory disease (PID) at times must be distinguished from acute pyelonephritis. Characteristic physical findings and negative urine cultures should make differentia­tion fairly easy.

In male patients with febrile genitourinary tract infection, the main differential diagnosis consists of acute pyelonephritis, acute prostatitis, and acute epididymoorchitis. Characteristic physical findings and symptoms in prostatitis and epididymitis should make this differentiation easy.

Acute pyelonephritis must be distinguished from renal abscess and perinephric abscess. Radiographic studies often are necessary to confirm the specific diagnosis.

Treatment                                                                                                      

 

Ambulatory younger women who present with signs and symptoms of uncomplicated acute pyelonephritis may be candidates for outpatient therapy. They must be otherwise healthy and must not be pregnant. In addition, they must be treated initially in the emergency department (ED) with vigorous oral or IV fluids, antipyretic pain medication, and a dose of parenteral antibiotics. Studies have shown that outpatient therapy for selected patients is as safe as inpatient therapy for a comparable group of patients and is much less expensive.

Use analgesics as needed. Early in the course of the illness, parenteral analgesics are often necessary to reduce morbidity from symptoms. Nonsteroidal anti-inflammatory drugs and narcotics are complementary; do not assume that one class is better than the other.

Admission is usually appropriate for patients who are severely ill, pregnant, or elderly or who have comorbid disorders that increase the complexity of management or the complication rate (eg, diabetes mellitus, chronic lung disease, congenital or acquired immunodeficiency). Admission may also be advisable for patients whose social situation is unstable, because of the possibility of poor compliance or poor follow-up.

Emergency surgery may be indicated in a patient with fever or positive blood culture results persisting longer than 48 hours; in a patient whose condition deteriorates; or in a patient who appears toxic for longer than 72 hours. These patients may have an abscess, emphysematous pyelonephritis, or an obstructing calculus. The etiology may not be immediately evident, but an unexpected change in the clinical picture warrants immediate evaluation for potential surgical intervention.

After recovery from the acute infection, patients may be candidates for elective surgery to reverse conditions that predispose the kidney to recurrent infections and renal damage. These conditions include congenital anomalies, fistulae involving the urogenital tract, prostatic hypertrophy, renal calculi, and vesicoureteral reflux.

 

 

 

 

 

 

A. Specific Measures: When the infection is se­vere or complicating factors are present, hospitalization may be required. Urine and blood specimens must be obtained immediately for culture; recognized pathogens must be tested for antimicrobial sensitivity. Until the results of these tests are known, antimicrobial drugs should be given empirically. Although clinicians differ in their choice of antimicrobial agents, our pref­erence is to administer an aminoglycoside (amikacin, gentamicin, or tobramycin) plus ampicillin intrave­nously in full dosage. If the pathogen is sensitive and the clinical response is favorable, this treatment is continued for about 1 week and then re­placed with an appropriate oral antimicrobial drug for an additional 2 weeks. Complicating factors, eg, obstructive uropathy or infected stones, must be rec­ognized early and dealt with effectively if complica­tions are to be avoided.

B. General Measures: Complete bed rest is ad­vised until symptoms subside. Medication should be given for pain, fever, and nausea. It is important to give fluids intravenously and orally to ensure adequate hydration and maintenance of adequate urinary output.

C. Failure of Response: If the clinical response remains poor after 48-72 hours of therapy, reevalua-tion is necessary to assess for possible complicating factors (eg, obstructive uropathy) or the use of inap­propriate drugs. Excretory urography is required; if this is contraindicated, retrograde urography must be done. Unless treated quickly and effectively, obstruc­tive uropathy complicating acute pyelonephritis can lead to bacteremia and irreversible renal damage.

 

 

              Ureteral catheterization

 

 

 

 

  PERCUTANEOUS NEPHROSTOMY

 

 

 

Antimicrobial Agents Used in the Treatment of Acute Pyelonephritis

 

 

Agent


Dosing schedule

Oral dose


IV dose


Comments

Amoxicillin

Every 8 to 12 hours

500

-

None

Amoxicillin- clavulanate potassium (Augmentin)

Every 8 to 12 hours

500/125

-

GI side effects*

Ampicillin-sulbactam
(Unasyn)

Every 4 to 6 hours

-

150 to 200 mg
per kg per day

GI side effects*

Aztreonam (Azactam)

Every 6 to 8 hours

-

1 to 2 g

Phlebitis; GI side effects*

Cefotaxime (Claforan)

Every 8 to 12 hours

-

1 to 2 g

Thrombophlebitis

Ceftriaxone (Rocephin)

Once in 24 hours

-

1 to 2 g

Leukopenia; elevated BUN

Cephalexin (Keflex)

Every 6 hours

500

-

GI side effects*

Ciprofloxacin (Cipro)

Every 12 hours

500

400 mg

Nausea; headache; photosensitivity; pregnancy category C

Norfloxacini

Every 12 hours

500

400 mg

Nausea; headache; photosensitivity; pregnancy category C

 

 

 

Regimens for complicated cases

 

With complicated acute pyelonephritis, treat patients parenterally until defervescence and improvement in the clinical condition warrants changing to oral antibiotics. Complete the course of therapy with an oral agent selected on the basis of culture results.Acceptable regimens include the following:

 

Ampicillin and an aminoglycoside

 

Cefepime

 

Imipenem

 

Meropenem

 

Piperacillin-tazobactam

 

Ticarcillin-clavulanate

 

If the patient is allergic to penicillin, it should be substituted with vancomycin. Vancomycin or linezolid are options if enterococci are a consideration.

 

 

 

 

D. Follow-Up Care: Clinical improvement does not always imply cure of the infection. In about one-third of patients, symptoms improve despite persis­tence of the bacterial pathogen. Therefore, repeat urine cultures are important during and after therapy for a follow-up period of at least 6 months.

 

Prognosis

When identified promptly and treated appropri­ately in a patient who has no underlying complicating factors, acute pyelonephritis carries a good prognosis for cure without sequels. The likelihood of serious sequels and a less favorable prognosis varies with the severity of complicating factors and the patient's age at the onset.

 

Possible Complications

Acute kidney failure

Kidney infection returns

Infection around the kidney (perinephric abscess)

Severe blood infection (sepsis)

 

Prevention

 

Prompt and complete treatment of bladder infections may prevent development of many cases of pyelonephritis. Chronic or recurrent urinary tract infection should be treated thoroughly.

 

You can help preventing kidney infections by taking the following steps:

Keep the genital area clean. Wiping from front to back helps reduce the chance of introducing bacteria from the rectal area to the urethra.

Urinating immediately after sexual intercourse. This may help eliminate any bacteria that may have been introduced during sexual activity.

Drink more fluids (64 to 128 ounces per day). This encourages frequent urination and flushes bacteria from the bladder.

Drink cranberry juice. Doing so prevents certain types of bacteria from attaching to the wall of the bladder and may lessen your chance of infection.

 

 

 

 

 

 

 

 

Gestation pyelonephritis.

(Pyelonephritis of pregnancy).

                   

 

Acute pyelonephritis is a bacterial infection of the kidneys, which affects 1 to 2% of pregnant women. In most cases, the infection first develops in the lower urinary tract. If not diagnosed and treated properly, the infection may ascend from the urethra and genital area to the bladder, then to one or both kidneys.

 

Compared to non-pregnant women, pregnant women are more likely to develop pyelonephritis. This is due to physiological changes during pregnancy that can interfere with the flow of urine. Normally, the ureters drain urine from the kidney into the bladder and out of the body through the urethra. But, during pregnancy, the high concentration of the hormone progesterone can inhibit contraction of these drainage ducts. Also, as the uterus becomes enlarged during pregnancy, it can compress the ureters. These changes can lead to problems with proper drainage of the urine from the kidneys, causing the urine to remain stagnant. As a result, bacteria in the bladder, rather than being washed out of the system, may migrate to the kidneys and cause infection. The Escherichia coli (E. Coli) bacterium is the usual culprit. Other bacteria-such as Klebsiella pneumoniae, Proteus species, and staphylococci-can also cause kidney infections. About 75 to 80% of cases of pyelonephritis occur on the right side, 10 to 15% are left-sided, and about 10% are bilateral.

Pyelonephritis is an infection of the uppermost section of the urinary tract. The condition is more common in women with asymptomatic urinary tract or bladder infection. Studies have identified a risk ratio of 14 to 1,000. This means about 14 cases of acute pyelonephritis are diagnosed per 1,000 pregnancies. It is estimated that up to 70-percent of cases can be avoided with regular urine cultures and subsequent treatment for bacterium present in urine. Treatment for urinary infections, including bladder infections and pyelonephritis, is a course of antibiotics.

 

Causes of Pyelonephritis

Pyelonephritis occurs more frequently in pregnant patients due to increased progesterone and pressure placed on the ureters by the growing uterus. In about 85-percent of cases, E. coli is the bacterium responsible for infection though other bacterium, including staphylococcus and group D streptococci may also be responsible.

 

The inflammatory process develops while pregnancy, delivery and puerperal period. Most frequently it is observed in pregnant (48%) more rare in puerperal (35%) women. It develops while 1 pregnancy 2 trimester often. There are women 18-25 years old. That is explained by a not complete adaptation to immunologic, hormone changes of the pregnancy. It is supposed not to be a primary disease but activation of latent pyelonephritis.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


Urinoculture finds out E.Coli, Staphylococcus albicans, Clebsiella in pregnant women. Association of the Proteus and Blue pus bacilli is observed in puerperal women. The primary source of the infection may be any purulent inflammatory place (furunculosis, dental caries, inflammatory diseases of the genital organs).

The pathogenetic sign is bacteriuria. It is observed in 7% only. Urodynamic dysfunction favors the pyelonephritis development. Pathogenesis may be explained with mechanical, neurohumoral and endocrine factors. The enlarged uterus compresses the pelvic portion of the ureters causing ureteropyeloectasia while pregnancy. Urostasis at the upper portion develops because of decreasing of the ureteral muscles and pelvises of the kidney tension.

The moderate hypotonia and hypokinesia of the calicopelvic of the both kidneys and ureters are observed on 8th week.

Changes of the upper portion of the urinary tract may be explained by weakening of the sympathetic nervous system tonus. Dysfunction of the urinary output because of the urinary pathway atonia is a condition for pathogen activation. Vesicoureteral and pelvicorenal refluxes favor spreading of the infection into the interstitial tissue of the renal parenchyma (medulla of the kidney).

Acute pyelonephritis of pregnancy. Primary acute process acute rarely. This is an active phase of the chronic process frequently. The prepueral women have attacks of the acute pyelonephritis at the 4-, 6-, 12- day of the puerperal period (these are days of the postpartum complications: endometritis, metrophlebitis).

Urinary tract infection

 

UTI is defined as the presence of at least 100,000 organisms per milliliter of urine in an asymptomatic patient, or as more than 100 organisms/mL of urine with accompanying pyuria (> 7 white blood cells [WBCs]/mL) in a symptomatic patient. A diagnosis of UTI should be supported by a positive culture for a uropathogen, particularly in patients with vague symptoms. UTIs are associated with risks to both the fetus and the mother, including pyelonephritis, preterm birth, low birth weight, and increased perinatal mortality.

 

Asymptomatic bacteriuria

Asymptomatic bacteriuria is commonly defined as the presence of more than 100,000 organisms/mL in 2 consecutive urine samples in the absence of declared symptoms. Untreated asymptomatic bacteriuria is a risk factor for acute cystitis (40%) and pyelonephritis (25-30%) in pregnancy. These cases account for 70% of all cases of symptomatic UTI among unscreened pregnant women.

 

Acute cystitis

Acute cystitis involves only the lower urinary tract; it is characterized by inflammation of the bladder as a result of bacterial or nonbacterial causes (eg, radiation or viral infection). Acute cystitis develops in approximately 1% of pregnant patients, of whom 60% have a negative result on initial screening. Signs and symptoms include hematuria, dysuria, suprapubic discomfort, frequency, urgency, and nocturia. These symptoms are often difficult to distinguish from those due to pregnancy itself.

 

Acute cystitis is complicated by upper urinary tract disease (ie, pyelonephritis) in 15-50% of cases.

 

Acute pyelonephritis

Pyelonephritis is the most common urinary tract complication in pregnant women, occurring in approximately 2% of all pregnancies. Acute pyelonephritis is characterized by fever, flank pain, and tenderness in addition to significant bacteriuria. Other symptoms may include nausea, vomiting, frequency, urgency, and dysuria. Furthermore, women with additional risk factors (eg, immunosuppression, diabetes, sickle cell anemia, neurogenic bladder, recurrent or persistent UTIs before pregnancy) are at an increased risk for a complicated UTI.

Risks of Other Pregnancy Complications Associated with Pyelonephritis

 

Untreated pyelonephritis may cause other pregnancy complications, including respiratory distress, anemia and impaired kidney function. About 20-percent of severe cases lead to septic shock with acute respiratory and kidney malfunction. About 5-percent of women with an acute form of the infection will suffer preterm delivery

 

 

 

Clinical findings.

Clinical findings have the own peculiarities according to the different terms of pregnancy. They also depend on the range of the urinary output damage. A sharp pain in loin that irradiates to the lower portions of the abdomen, genitals are at the 1 trimester. 2nd and 3rd trimesters are characterized with a moderate pain because of the dilatation of the upper urinary tract and intrarenal pressure decreasing.

An acute purulent pyelonephritis develops more frequently in pregnant and postpueral women. There is a high lethality rate caused by an acute purulent pyelonephritis.

 

Diagnosis is rather difficult. The enlarged uterine hinders the palpation. The right kidney damage should be differed from the acute appendicitis and cholecystitis.

 

 

 Ultrasonography (shows dilatation of the calyces and renal pelvis, dysfunction of the urine passages, edema of the adipose capsule looks as rarefaction about the kidney)

 

 

 Ultrasonography

 

 

 

 

 

X-ray imaging is inadmissible exclusive rare occasions.

 

          Chromocystoscopia

 

The endoscopy investigation isn’t recommended too. In case of the suspicion of purulent process the complete clinical research is required including Chromocystoscopia, radionuclide renography, scanning, excretory urography, ultrasonography. The delayed excretion of the indigocarmine while Chromocystoscopia is attended to peculiar urodynamic due to pregnant uterus.

 

 

Treatment.                                                                                

Caesar’s incision by retroperitoneal access is performed because of an acute inflammation at the last days of pregnancy.

Antibiotics shouldn’t be harmful to fetus. The natural and semisynthetic penicillines are recommended at the 1st trimester. Wider choice of antibiotics is at the 2nd and 3rd trimesters because placenta has its barrier function then.

The puerperal women may transfer drugs to child with milk.

Treatment should be continuous. Nitrofuranes are admissible after 2nd month in dosage 50-100mg per day. Nalidixone acid is admissible after the 4th month of pregnancy (2g per day for 2-3 weeks). But its administration must be stopped before delivery.

 

 

Table. Treatment of Pyelonephritis During PregnancyMild to moderate pyelonephritis

 

ceftriaxone (Rocephin) 1 g IV q24h or

 

cefepime (Maxipime) 1 g IV q12h or

 

cefotaxime (Claforan) 1-2 g IV q8h or

 

ceftazidime (Fortaz, Tazicef) 2 g IV q8h or

 

ampicillin 1-2 g IV q6h plus gentamicin IV 1.5 mg/kg q8h

Severe pyelonephritis

If patient is immunocompromised and/or has incomplete urinary drainage:

 

ticarcillin-clavulanate (Timentin) 3.1 g IV q6h or

 

ampicillin-sulbactam (Unasyn) 1.5 g IV q6h or

 

piperacillin-tazobactam (Zosyn) 3.375 g IV q6h

 

 

 

 

 

 

 

 

  Ureteral catheterization

 

 

The acute purulent pyelonephritis in pregnant women requires the obligate surgical measures. Its scope depends on form of the disease. It is necessary anyway until the delivery.

Approximately 20 to 30% of pregnant patients with pyelonephritis develop recurrent infections later in pregnancy. The most cost-effective way to lower your risk of recurrence is to take a single dose of an antibiotic daily, as a preventive measure. Sulfisoxazole (Gantrisin), 1g, or nitrofurantoin monohydrate macrocrystals (Macrobid), 100 mg, are appropriate options.

 

Prognosis

In most cases of bacteriuria and urinary tract infection (UTI) in pregnancy, the prognosis is excellent. The majority of long-term sequelae are due to complications associated with septic shock, respiratory failure, and hypotensive hypoxia (ie, extremity gangrene).

 

Maternal UTI has few direct fetal sequelae because fetal bloodstream infection is rare; however, uterine hypoperfusion due to maternal dehydration, maternal anemia, and direct bacterial endotoxin damage to the placental vasculature may cause fetal cerebral hypoperfusion.

Untreated upper UTIs are associated with low birth weight, prematurity, premature labor, hypertension, preeclampsia, maternal anemia, and amnionitis. A retrospective population-based study by Mazor-Dray et al showed that UTI during pregnancy is independently associated with intrauterine growth restriction, preeclampsia, preterm delivery, and cesarean delivery.

 

 

 

 

RENAL ABSCESS (Renal Carbuncle)

 

 

 

 

                                  

An abscess is a localized collection of pus in a hollow area formed by the breaking up of tissues. A renal abscess is one that is confined to the kidney and is caused either by bacteria from an infection traveling to the kidneys through the bloodstream or by a urinary tract infection traveling to the kidney and then spreading to the kidney tissue.

A renal abscess is a very unusual disease, but generally occurs as a result of common problems such as kidney inflammation, stone disease and vesicoureteral reflux. Occasionally, a renal abscess can develop from a source of infection in any area of the body. Multiple skin abscesses and intravenous drug abuse can also be sources of renal abscess. Complicated urinary tract infections associated with stones, pregnancy, neurogenic bladder and diabetes mellitus also put a person at risk for renal abscess.

 

 

Etiology

Renal cortical abscesses develop primarily as a result of hematogenous spread of Staphylococcus aureus infections at distant sites (most often the skin). At times, foci of primary renal infections caused mainly by gram-negative bacteria (coliform organisms) coalesce in the renal medulla to form abscesses. In the past, most renal abscesses were caused by staphylococci; recently, coliform bacteria have become the predominant pathogens in renal abscesses. Renal abscesses caused by obligate anaerobic bacteria are rare.

 

 

 

 

        Pathogenesis & Pathology 

                               

 

An abscess (carbuncle) caused by S aureus de­velops from hematogenous spread of the organism from a primary skin lesion. Intravenous drug abusers are especially prone to develop staphylococcal renal abscesses. Multiple focal abscesses evolve and even­tually coalesce to form a multilocular abscess. Un­treated cortical abscesses may rupture into the pyelocaliceal system or into the perinephric space (perinephric abscess). Urinary tract infection occurs only if the abscess communicates with the pyelocaliceal sys­tem.

The more common type, renal medullary abscess, evolves from acute or chronic foci of pyelonephritis, often associated with ureteral obstruction or calculous disease (calculous pyonephrosis). The infecting pathogens usually are gram-negative rods. Timmons and Perlmutter (1976) believe that gram-negative bacillary abscesses in children may be a complication of vesicoureteral reflux, with the pathogens invading the collecting tubules. In adults, the kidney usually is damaged by chronic suppurative pyelonephritis that may culminate in one or more abscesses. Medullary abscesses may also rupture into the perinephric space. One-third of affected patients are diabetics.

 

 

Clinical Findings

A. Symptoms: Staphylococcal renal abscess is typified by an abrupt onset of chills, fever, and lo­calized costovertebral pain. In the early stages, when the abscess does not communicate with the collecting system, symptoms of vesical irritability are absent and urinalysis is normal, although the patient may appear quite septic. The clinical picture often mimics that of acute pyelonephritis.

In most patients with medullary abscesses due to gram-negative rods, there is a history of persistent or recurrent bouts of urinary tract infection, often as­sociated with urolithiasis, obstructive uropathy, or renal surgery.

B. Signs: In acute cases, localizing signs are flank tenderness, possibly a palpable mass, and erythema and edema of the skin of the overlying loin. At times, however, abscesses associated with both acute and chronic infections present as febrile illnesses with few localizing signs.

C. Laboratory Findings: The hemogram usu­ally shows marked leukocytosis with a shift to the left. With cortical abscesses that do not communicate with the collecting system, urinalysis shows no pyuria or bacteriuria, and urine culture is negative. Medullary abscesses generally are associated with heavy pyuria, bacteriuria, and positive urine cultures. The sudden appearance of heavy pyuria and bacteriuria may herald the rupture of a previously noncommunicating abscess into the collecting system. Blood cultures may be positive.

Depending upon the extent of renal involvement and associated renal abnormalities, the serum creatinine and urea nitrogen values may be normal or elevated. Since patients with renal abscesses often are diabetic, glycosuria and hyperglycemia may be found.

D. X-Ray Findings: If the renal outline is visi­ble, the plain film may show an enlarged kidney or a bulge of the external renal contour. With perinephric edema, however, often the renal outline is obliterated and the psoas shadow indistinct. Unless the abscess has ruptured into the perinephric space or is quite large, scoliosis generally is not observed. Renal stones may be noted. When cortical abscesses are small, the excretory urogram may appear normal; most often, however, a space-occupying lesion (the abscess) is delineated. Pyelonephritic changes, hydronephrosis, and urolithiasis also may be observed. Delayed opacification or even a nonfunctioning kidney may be found.

   Excretory urogram

 

 

 

 

 

 

                          KUB    

      Excretory urogram

 

Renal angiography usually makes the diagnosis. The abscess fails to opacify; its walls are irregular. Surrounding vessels are displaced, and hypervascularity is common. The most important sign is excessive capsular vessels overlying the abscess.

 

E. Ultrasonography:

 

 Ultrasonography

 

 Renal echograms gener­ally distinguish simple cysts (no internal echoes) from solid masses (many internal echoes) but often fail to distinguish renal abscesses from malignant lesions, particularly necrotic, cystic renal cell carcinomas. Percutaneous needle aspiration of the mass under ul­trasonic guidance may confirm the diagnosis.

 

 

 

 

 

   CT Scans

 

F. CT Scans: Experience has been limited in the utilization of CT scans for the diagnosis of renal ab­scess. The attenuation coefficient value (CT number) varies considerably with the amount of liquid pus or solid debris within the abscess, and abscesses cannot be differentiated from hemorrhagic cysts or solid neo­plasms with certainty. Percutaneous needle aspiration of the mass under CT control may confirm the diag­nosis.

 

 

 

   CT Scans

 

 

 

 

G. Isotope Scanning: The rectilinear scan will depict a space-occupying lesion. With the use of technetium and iodine compounds, the Anger camera will show an avascular mass lesion. These findings also are compatible with simple cyst. Gallium-67 localizes in inflammatory tissue; an ab­scess will therefore "light up" on dynamic scanning.

Gallium scanning may demonstrate an abscess even when excretory urograms are normal.

Differential Diagnosis

In acute pyelonephritis, symptoms and signs may be similar to those of abscess; however, no space-occupying lesion is shown on the urogram, and a gallium scan will not show an abscess.

When symptoms of vesical irritability are absent and urinalysis is normal, renal abscess may be con­fused with acute cholecystitis. The presence of a pal­pable and tender gallbladder may make the diagnosis. Radiographic visualization of the gallbladder and kid­neys should be definitive.

Acute appendicitis may be confused with renal abscess, because renal pain often radiates to the lower abdominal quadrant. The findings on physical exami­nation, laboratory studies, and radiographic studies should allow differentiation.

At times, renal cell carcinoma may be confused with renal abscess, especially when there is fever re­lated to tumor necrosis. Radiographic studies and scans usually will allow differentiation; however, per­cutaneous needle aspiration may be required in some cases.

Complications

Complications of renal abscess include both bacteremia with generalized sepsis and rupture of the abscess into the perinephrium.

 

 

 

Treatment              

 

In most patients with acute focal or multifocal pyelonephritis, treatment with appropriate antibiotics should produce a clinical response within one week of initiating therapy. However, well-established large abscesses are often difficult to treat with antibiotics alone, with most studies limiting treatment of renal abscesses with antibiotics alone to lesions smaller than 3 cm.

 

In most patients with suspected corticomedullary abscess, a prompt attempt at treatment with intravenous antibiotics directed against culture-specific bacteria in addition to intravenous fluid resuscitation may be used. Medical treatment alone should be limited to hemodynamically stable patients with small (< 3 cm) corticomedullary abscesses. Patients with signs of hemodynamic instability due to sepsis or with large renal abscesses (≥3 cm) should undergo percutaneous or surgical drainage for abscess management (see Surgical Care). Moreover, medical therapy alone in the treatment of perinephric abscesses is inappropriate, as the risk of mortality associated with perinephric abscess treated with antibiotics alone is upward of 33%.

 

Intravenous administration of a penicillin derivative, a cephalosporin, an aminoglycoside, or a fluoroquinolone is the appropriate initial medical treatment. Following sufficient resolution of nausea/vomiting and fever, antibiotics may be administered orally.

 

For combination therapy, a beta-lactam antibiotic plus an aminoglycoside should be administered intravenously. Administer this line of therapy until culture and sensitivity results are received and then modify the antimicrobial therapy to the most appropriate agent.

 

The duration of therapy is not well defined. Continue parenteral antibiotics for at least 24-48 hours after patient symptoms clinically improve and the fever resolves. Then, administer a suitable oral antibiotic medication and continue this treatment regimen for an additional 2-4 weeks, as determined by complete clinical and radiographic resolution of the intrarenal process.

 

Factors that may contribute to medical treatment failure include elderly age, diabetes mellitus, large abscesses, obstructive uropathy, and urosepsis.

Treatment calls for immediate intravenous administration of broad-spectrum antibiotics and drainage of the abscess. The drainage technique depends on the size and location of the abscess. Smaller, isolated lesions may be drained with a needle inserted through the skin (percutaneous aspiration) under ultrasound guidance. For simple, one-cavity (unilocular) abscesses within the kidney, drainage is done through a small tube (catheter drainage). If the abscess is large, located in certain areas of the kidney (renal cortex), or the patient is older and septic, open surgical drainage may be necessary. Sometimes it is not possible to save the kidney and removal of part or all of the kidney (simple, partial, or complete nephrectomy) may be necessary.

 

Antimicrobial therapy alone is not indicated for patients with xanthogranulomatous pyelonephritis (XGP). Nephrectomy is required.

 

    NEPHROSTOMY

 

 

Drainage by percutaneous means or surgical incision may be necessary. Relief of complicating urinary obstruction is mandatory. Nephrectomy and partial nephrectomy are required less often today than in the past.

 

 

Prognosis

The outlook is good provided the diagnosis is made promptly and effective therapy is instituted im­mediately.

 

 

 

PERINEPHRIC ABSCESS

 

Etiology

Perinephric abscesses lie between the renal cap­sule and the perirenal (Gerota's) fascia. Most result from rupture of an intrarenal abscess into the perinephric space; the causative organisms are usually coliform bacteria and Pseudomonas, less often staphylococci and obligate anaerobes.

Pathogenesis & Pathology

Staphylococcal perinephric abscesses probably originate from rupture of a small renal cortical abscess or, less commonly, from a renal carbuncle. The pri­mary renal lesion may heal, although the perinephric abscess progresses.

Usually, however, perinephric cellulitis and ab­scess complicate severe renal parenchymal infection caused by gram-negative bacteria in association with calcufous pyonephrosis or infected hydronephrosis. It is presumed that spontaneous extravasation of infected material occurs. In this instance, pus and bacteria usually are found in the urine.

Perinephric abscesses may become quite large. When advanced, they tend to point over the iliac crest (Petifs triangle) posterolaterally.

 

Clinical Findings                           

A. Symptoms: The most common symptoms of perinephric abscess include chills, fever, unilateral flank pain, and abdominal pain. Malaise and prostra­tion occur variably. Only about one-third of patients complain of dysuria.

B. Signs: Fever tends to be low-grade unless generalized sepsis evolves. There is usually marked tenderness over the affected kidney and costovertebral angle. A large mass may be felt or percussed in the flank. Abdominal tenderness accompanied by variable rebound tenderness may be elicited. The diaphragm on the affected side may be elevated and fixed. Ipsilateral pleural effusion is common. Scoliosis with the concav­ity to the affected side usually is seen; this results from spasm of the psoas muscle, which also causes the patient to lie with the ipsilateral leg flexed on the abdomen. Erythema and edeina of the overlying skin may be evident. Minimal edema is best demonstrated by having the patient lie on a rough toweLfor a few minutes.

 

C. Laboratory Findings: Leukocytosis is usual but may be mild; a shift to the left is commonly seen. The erythrocyte sedimentation rate usually is elevated; anemia may be present. Pyuria and bacteriuria are found commonly but not routinely. Blood cultures may be positive. Unless bilateral renal disease is pres­ent, the serum creatinine and blood urea nitrogen values generally are normal.

 

 Plain film (stoun in the left kidney)

 

D. X-Ray Findings: A plain film of the abdomen typically shows evidence of a flank mass. Surrounding edema often results in obliteration of the renal and psoas shadows on the affected side. Scoliosis with the concavity to the affected side is common. The pres­ence of a calcified body in this area suggests an abscess resulting from calculous pyonephrosis. Occasionally, a localized collection of gas caused by infection with gas-forming (coliform) organisms may be observed in the perirenal area.

       Excretory urogram

                                                     

Excretory urograms may show delayed visualiza­tion or nonfunction related to obstructive uropathy or parenchymal disease. Changes suggesting a space-occupying lesion (eg, carbuncle) may be noted; how­ever, evidence of advanced hydronephrosis or calcu­lous pyonephrosis is seen most commonly. Lack of mobility of the kidney with change in position of the patient or with respiration strongly suggests acute or chronic perinephritis. The entire kidney or only one pole may be displaced laterally by the abscess.

A barium enema may show displacement of the bowel anteriorly, laterally, or medially. Paralytic ileus may be observed on plain films of the abdomen or on upper gastrointestinal series. Chest films may demonstrate an elevated dia­phragm on the ipsilateral side; fluoroscopy often shows fixation on respiration. Some free pleural fluid and platelike atelectasis may be observed.

When the findings of excretory urography are equivocal, the performance of retrograde urograms may be helpful.

Gallium-67 localizes in inflammatory tissue; hence, the diagnosis often may be confirmed by use of the scintillation camera.

Echograms, CT scans, and renal angiograms may assist in diagnosis, especially when combined with percutaneous needle aspiration.

 

Differential Diagnosis

Acute renal infections cause many of the symp­toms that accompany perinephric abscess: fever, lo­calized pain, and tenderness. In acute pyelonephritis, the urine uniformly shows evidence of infection; in perinephric abscess, the urine may or may not show evidence of infection. X-ray studies and scans, how­ever, should facilitate differentiation of these 2 condi­tions.

Infected hydronephrosis may cause fever and lo­calized pain and tenderness and may account for the presence of a flank mass. Again, x-ray studies and scans should make the differentiation.

Paranephric abscess is a collection of pus external to the perirenal fascia and often is secondary to in­flammatory disease of the spine (eg, tuberculosis). Many of the signs of perinephric abscess may be seen on a plain x-ray film, but the finding of a lesion in bone in the low thoracic area should suggest the correct diagnosis. Urograms are normal.

Complications

Unless the correct diagnosis is made promptly and effective therapy is initiated early, the mortality rate from generalized sepsis is quite high. Rarely, the perinephric abscess may point just above the iliac crest posterolaterally or extend downward into the iliac fossa and inguinal region. It is most unusual for the phlegmon to extend within the perirenal fascia across the midline to involve the opposite side of the body.

The abscess may produce considerable ureteral compression, giving rise to hydronephrosis. Even after drainage of the abscess, ureteral stenosis from periureteritis may evolve during the healing process.

Prevention

Early, effective treatment of urinary tract disease is the only means of preventing perinephric abscess. Appropriate therapy of urinary tract infection and re­moval of calculi and other obstructive conditions are of highest priority.

 

Treatment

Generally, treatment is similar to treatment for renal abscesses, except that surgical drainage usually is required for perinephric abscesses but may not be required for intrarenal abscesses. Intensive antimi­crobial therapy, based upon culture and sensitivity testing of the pathogen isolated from urine, blood, or pus obtained by needle aspiration of the lesion, is mandatory. Unless adequate percutaneous drainage can be established, surgical drainage usually is needed. Because of underlying renal disease, nephrectomy may be required, either acutely or subsequent to initial control of the abscess. When nephrectomy is not required—indeed, even if the kidney itself is nor­mal—excretory urography should be performed about 3 montns after therapy is completed to make certain that late complications (eg, ureteral stenosis) are not missed.

Prognosis

Perinephric abscess often is fatal when diagnosis and appropriate therapy are delayed. A high index of suspicion and improved methods of diagnosis and treatment should offer a better prognosis than the 44% mortality rate observed by Thorley, Jones, and San-ford (1974).

 

 

 

 

                                                                        TUBERCULOSIS   

 

Tuberculosis, or TB, primarily affects the lungs but the causative bacteria, Mycobacterium tuberculosis, can spread to other parts of the body, including the kidneys, bladder and urinary tract. Urinary tuberculosis can arise because the tuberculosis virus directly invades the kidneys or lower urinary tract, or it can result from urinary system deposits of the protein amyloid, formed when tuberculosis destroys other body tissues.   

 

Tubercle bacilli may invade one or more (or even all) of the organs of the genitourinary tract and cause a chronic granulomatous infection that shows the same characteristics as tuberculosis in other organs. Urinary tuberculosis is a disease of young adults (60% of pa­tients are between the ages of 20 and 40) and is a little more common in males than in females.

Etiology

The infecting organism is Mycobacterium tuber­culosis, which reaches the genitourinary organs by the hematogenous route from the lungs. The primary site is often not symptomatic or apparent.

The kidney and possibly the prostate are the pri­mary sites of tuberculous infection in the genitourinary tract. All other genitourinary organs become involved either by ascent (prostate to bladder) or descent (kid­ney to bladder; prostate to epididymis). The testis may become involved by direct extension from epididymal infection.

 

Pathogenesis

                                                  

A. Kidney and Ureter: When a shower of tuber­cle bacilli hits the renal cortex, the organisms may be destroyed by normal tissue resistance. Evidence of this is commonly seen in autopsies of persons who have died of tuberculosis; only scars are found in the kid­neys. However, if enough bacteria of sufficient viru­lence become lodged in the kidney and are not over­come, a clinical infection is established.

Tuberculosis of the kidney progresses slowly; it may take 15-20 years to destroy a kidney in a patient having good resistance to the infection. As a rule, therefore, there is no renal pain and little or no clinical disturbance of any type until the lesion has involved the calices or the pelvis, at which time pus and or­ganisms may be discharged into the urine. It is only at this stage that symptoms (of cystitis) are manifested. The infection then proceeds to the pelvic mucosa and the ureter, particularly its upper and vesical ends. This may lead to stricture and back pressure (hydronephrosis).

As the disease progresses, a caseous breakdown of tissue occurs until the entire kidney is replaced by cheesy material. Calcium may be laid down in the reparative process. The ureter undergoes fibrosis and tends to be shortened and therefore straightened. This change leads to a "golf-hole" (gaping) ureteral orifice, typical of an incompetent valve.

 

 

                

 

B. Bladder: Vesical irritability develops as an early clinical manifestation of the disease as the blad­der is bathed by infected material. Tubercles form later, usually in the region of the involved ureteral orifice, and finally coalesce and ulcerate. These ulcers may bleed. With severe involvement, the bladder be­comes fibrosed and contracted; this leads to marked frequency. Ureteral reflux or stenosis and, therefore, hydronephrosis may develop. If contralateral renal in­volvement occurs later, it is probably a separate hema­togenous infection.

 

C. Prostate and Seminal Vesicles:      

The passage of infected urine through the prostatic urethra will ultimately lead to invasion of the prostate and one or both seminal vesicles. There is no local pain.

On occasion, the primary hematogenous lesion in the genitourinary tract is in the prostate. Prostatic in­fection can ascend to the bladder and descend to the epididymis.

D. Epididymis and Testis: Tuberculosis of the prostate can extend along the vas or through the perivasal lymphatics and affect the epididymis. Because this is a slow process, there is usually no pain. If the epididymal infection is extensive and an abscess forms, it may rupture through the scrotal skin, thus establishing a permanent sinus, or it may extend into the testicle.

Pathology

A. Kidney and Ureter: The gross appearance of the kidney with moderately advanced tuberculosis is often normal on its outer surface, although it is usually surrounded by marked perinephritis. Usually, how­ever, there is a soft, yellowish localized bulge. On section, the involved area is seen to be filled with cheesy material (caseation). Widespread destruction of parenchyma is evident. In otherwise normal tissue, small abscesses may be seen. The walls of the pelvis, calices, and ureter may be thickened, and ulceration appears frequently in the region of the calices at the point at which the abscess drains. Ureteral stenosis may be complete, causing "autonephrectomy." Such a kidney is fibrosed and functionless. Under these circumstances, the bladder urine may be normal and symptoms absent.

Microscopically, the caseous material is seen as an amorphous mass. The surrounding parenchyma shows fibrosis with tissue destruction, small round cell and plasma cell infiltration, and epithelial and giant cells typical of tuberculosis. Acid-fast stains will usu­ally demonstrate the organisms in the tissue. Similar changes can be demonstrated in the wall of the pelvis and ureter.

In both the kidney and ureter, calcification is common. It may be macroscopic or microscopic. Such a finding is strongly suggestive of tuberculosis but, of course, is also observed in bilharzial infection. Sec­ondary renal stones occur in 10% of patients.

In the most advanced stage of renal tuberculosis, the parenchyma may be completely replaced by ca­seous substance or fibrous tissue. Perinephric abscess may develop, but this is rare.

B. Bladder: In the early stages, the mucosa may be inflamed, but this is not a specific change. The bladder is quite resistant to actual invasion.

  Cystoscopy

 

Later, tubercles form and can be seen easily, especially through the cystoscope, as white or yellow raised nodules surrounded by a halo of hyperemia. With severe vesical contracture, reflux may occur.

 

 

                      Yellow raised nodules surrounded by a halo of hyperemia

 

 

Microscopically, the nodules are typical tuber­cles. These break down to form deep, ragged ulcers. At this stage the bladder is quite irritable. With heal­ing, fibrosis develops that involves the muscle wall.

 

C. Prostate and Seminal Vesicles: Grossly, the exterior surface of these organs may show nodules and areas of induration from fibrosis. Areas of necrosis are common. In rare cases, healing may end in calcifica­tion. Large calcifications in the prostate should suggest tuberculous involvement.

 

D. Spermatic Cord, Epididymis, and Testis: The vas deferens is often grossly involved; fusiform swellings represent tubercles. The epididymis is en­larged and quite firm. It is usually separate from the testis, although occasionally it may adhere to it. Microscopically, the changes typical of tuberculosis are seen. Tubular degeneration may be marked.

The testis is usually not involved except by direct extension of an abscess in the epididymis.

 

 

 

Clinical Findings                             

                              

Tuberculosis of the genitourinary tract should be considered in the presence of any of the following situations: (1) chronic cystitis that refuses to respond to adequate therapy, (2) the finding of pus without bac­teria in a methylene blue stain or culture of the urinary sediment, (3) gross or microscopic hematuria, (4) a nontender, enlarged epididymis with a beaded or thickened vas, (5) a chronic draining scrotal sinus, or (6) induration or nodulation of the prostate and thickening of one or both seminal vesicles (especially in a young man). A history of present or past tuber­culosis elsewhere in the body should cause the physi­cian to suspect tuberculosis in the genitourinary tract when signs or symptoms are present.

The diagnosis rests upon the demonstration of tubercle bacilli in the urine by culture. The extent of the infection is determined by (1) the palpable findings in the epididymides, vasa deferentia, prostate, and seminal vesicles; (2) the renal and ureteral lesions as revealed by excretory urograms; (3) involvement of the bladder as seen through the cystoscope; (4) the degree of renal damage as measured by loss of func­tion; and (5) the presence of tubercle bacilli in one or both kidneys.

 

A. Symptoms: There is no classic clinical picture of renal tuberculosis. Most symptoms of this disease, even in the most advanced stage, are vesical in origin (cystitis). Vague generalized malaise, fatigability, low-grade but persistent fever, and night sweats are some of the nonspecific complaints. Even vesical ir­ritability may be absent, in which case only proper collection and examination of the urine will afford the clue. Active tuberculosis elsewhere in the body is found in less than half of patients with genitourinary tuberculosis.

 

1. Kidney and ureter - Because of the slow pro­gression of the disease, the affected kidney is usually completely asymptomatic. On occasion, however, there may be a dull ache in the flank. The passage of a blood clot, secondary calculi, or a mass of debris may cause renal and ureteral colic. Rarely, the presenting symptom may be a painless mass in the abdomen.

 

2. Bladder-The earliest symptoms of renal tuberculosis may arise from secondary vesical in­volvement. These include burning, frequency, and nocturia. Hematuria is occasionally found and is of either renal or vesical origin. At times, particularly in a late stage of the disease, the vesical irritability may become extreme. If ulceration occurs, suprapubic pain may be noted when the bladder becomes full.

 

3. Genital tract-Tuberculosis of the prostate and seminal vesicles usually causes no symptoms. The first clue to the presence of tuberculous infection of these organs is the onset of a tuberculous epididymitis.

Tuberculosis of the epididymis usually presents as a painless or only mildly painful swelling. An ab­scess may drain spontaneously through the scrotal wall. A chronic draining sinus should be regarded as tuberculous until proved otherwise. In rare cases, the onset is quite acute and may simulate an acute nonspecific epididymitis.

Dysuria

Dysuria means painful or difficult urination. Urinary tuberculosis can cause a burning or gripping sensation during urination. Patients may feel an urge to urinate but be unable to. Many other conditions, including a run-of-the-mill urinary tract infection, can cause dysuria, so this symptom is not helpful in diagnosing urinary TB.

Hematuria

Hematuria means blood in the urine. The urine might carry a pinkish tinge that the patient can identify as blood, or the contamination might be visible only to a doctor checking urine under the microscope. Even a few drops of blood can discolor urine, so hematuria should not unduly worry the patient. As with dysuria, many conditions other than urinary TB can cause hematuria.

Pain

Patients with urinary TB typically complain of pain along the side between the last rib and the top of the hip, known as the flank. Flank pain is a common sign in many conditions that affect the kidneys. Patients often have back pain too, according to the Merck Manuals Online Medical Library.

Abscess

Tuberculosis infection can spread from the kidney into the space surrounding it. The infection can spread to the psoas muscle, running from the lower back to the thigh. Sometimes infection of the psoas causes an abscess on the front of the thigh.

Kidney Failure

According to Drs. Golden and Vikram in their November 2005 paper in "American Family Physician," urinary tuberculosis usually does not affect kidney function. The exception occurs with tuberculous interstitial nephritis, or inflammation in the spaces between the kidney tubules, which interferes with filtration and can shut down the kidneys

 

 

B. Signs: Evidence of extragenital tuberculosis may be found (lungs, bone, lymph nodes, tonsils, intestines).               

 

 

                  

 

1. Kidney-There is usually no enlargement or tenderness of the involved kidney.

2. External genitalia-A thickened, nontender, or only slightly tender epididymis may be discovered. The vas deferens often is thickened and beaded. A chronic draining sinus through the scrotal skin is almost pathognomonic of tuberculous epididymitis. In the more advanced stages, the epididymis cannot be differentiated from the testis upon palpation. This may mean that the testis has been directly invaded by the epididymal abscess.

Hydrocele occasionally accompanies tuberculous epididymitis. The "idiopathic" hydrocele should be tapped so that underlying pathologic changes, if pres­ent, can be evaluated (epididymitis, testicular tumor). Involvement of the penis and urethra is rare.

3. Prostate and seminal vesicles-These organs may be normal to palpation. Ordinarily, however, the tuberculous prostate shows areas of induration, even nodulation. The involved vesicle is usually indurated, enlarged, and fixed. If epididymitis is present, the ipsilateral vesicle usually shows changes as well.

C. Laboratory Findings: Proper urinalysis af­fords the most important clue to the diagnosis of genitourinary tuberculosis.

1. Persistent pyuria without organisms on culture or on the smear stained with methylene blue means tuberculosis until proved otherwise. Acid-fast stains done on the concentrated sediment from a 24-hour specimen are positive in at least 60% of cases. How­ever, this must be corroborated by a positive culture.

About 15-20% of patients with tuberculosis have secondary pyogenic infection; the clue ("sterile" pyuria) is thereby obscured. If clinical response to adequate treatment fails and pyuria persists, tuber­culosis must be ruled out by bacteriologic and roentgenologic means.

2. Cultures for tubercle bacilli from the first morning urine are positive in a very high percentage of cases of tuberculous infection. If positive, sensitivity tests should be ordered. In the face of strong presump­tive evidence of tuberculosis, negative cultures should be repeated.

The blood count may be normal or may show anemia in advanced disease. The sedimentation rate is usually accelerated.

Tubercle bacilli may often be demonstrated in the secretions from an infected prostate. Renal function will be normal unless there is bilateral damage: as one kidney is slowly injured, compensatory hypertrophy of the normal kidney develops. It can also be infected with tubercle bacilli, or it may become hydronephrotic from fibrosis of the7bladder wall (ureterovesical stenosis) or vesicoureteral reflux.

If tuberculosis is suspected, perform the tubercu­lin test. A positive test, particularly in an adult, is hardly diagnostic; but a negative test in an otherwise healthy patient speaks against a diagnosis of tuber­culosis.

 

D. X-Ray Findings: A chest film that shows evidence of tuberculosis should cause the physician to suspect tuberculosis of the urogenital tract in the presence of urinary signs and symptoms. A plain film of the abdomen may show enlargement of one kidney or obliteration of the renal and psoas shadows due to perinephric abscess. Punctate calcification in the renal parenchyma may be due to tuberculosis.

 

            KUB

 

Plain Radiographs

Plan radiographs of the urinary tract are important because they show calcification in the kidneys and in the lower genitourinary tract. Ureteral calcification is very uncommon. Calcification rarely occurs in the bladder wall and seminal vesicles except in advanced disease.

 

 

 

 

 

    

            Excretory urogram  

 

Intravenous Urography (IVU)

 

High dose IVU has traditionally been the gold standard tool to diagnose and evaluate genitourinary TB. It is still in practice but in many institutions has been replaced by spiral CT. IVU findings are distortion of calyx, ureteral dilation above a UVJ stricture or a rigid fibrotic ureter with multiple strictures. The cystographic phase of the IVU can give valuable information about the condition of the bladder, which may be small and contracted (thimble bladder) or with filling defects.

 

Computed Tomography

 

Spiral CT has arguably replaced IVU as the imaging modality of choice for the diagnosis because of 3 dimensional reconstructed images. It is equal to IVU in identifying calyceal abnormalities, hydronephrosis or hydroureter, autonephrectomy, amputated infundibulum, urinary tract calcifications, and renal parenchymal cavities.

 

Ultrasonography

It is of limited value, though used for initial screening and follow up.   

 

Renal stones are found in 10% of cases. Calcification of the ureter may be noted, but this is rare. Small prostatic stones the size of grape seeds in the region of the pubic symphysis are ordinarily not due to tuberculosis, but large calcific bodies may be.

Excretory urograms can be diagnostic if the lesion is moderately advanced. The typical changes include (1) a "moth-eaten" appearance of the involved ulcer­ated calices, (2) obliteration of one or more calices, (3) dilatation of the calices due to ureteral stenosis from fibrosis, (4) abscess cavities that connect with calices, (5) single or multiple ureteral strictures, with second­ary dilatation, with shortening and therefore straightening of the ureter, and (6) absence of function of the kidney due to complete ureteral occlusion and renal destruction (autonephrectomy).

       Excretory urogram

 

If the excretory urograms demonstrate gross tuberculosis in one kidney, there is no need to do a retrograde urogram on that side. In fact, there is at least a theoretical danger of hematogenous or lymphogenous dissemination resulting from the increased intrapelvic pressure.

 

        Retrograde urography

 

 Retrograde urography may, how­ever, be carried out on the unsuspected side as a verifi­cation of its normality. This is further substantiated if the urine from that side is free of both pus cells and tubercle bacilli.

 

Retrograde pyelography

Indications: 1. stricture at the lower end of the ureter, 2. Ureteral catheterization to obtain urine samples for culture from each kidney.

 

Percutaneous Antegrade Pyelography

It is an alternative to retrograde pyelography to aspirate contents of the renal pelvis or from the tuberculous cavities to estimate the quantity of drugs that has penetrated the walls.

It can also be used for percutaneous nephrostomy tube placement in an obstructive system.

 

Arteriography, Radioisotope Investigation, and Magnetic Resonance Imaging are rarely indicated as they do not provide any additional information above imaging modalities.

 

 

 

E. Instrumental Examination:  Cystoscopy and Biopsy

 

Cystoscopy is rarely indicated however in some place it is used in assessing the extent of disease or the response to chemotherapy.

Biopsy is usually necessary to rule out malignancy and is not advised before the initiation of medical therapy.

 

 Cystoscopic view

 

 Thorough cystoscopic study is indicated even when the offending organism has been found in the urine and excretory urograms show the typical renal lesion. This will clearly demonstrate the extent of the disease. Cystoscopy may reveal the typical tubercles or ulcers of tuberculosis. Biopsy can be done if necessary. Severe contracture of the bladder may be noted. A cystogram may reveal ureteral reflux. A clean specimen of urine should also be obtained for further study.

 

  Classification 

 I — nondestructive (infiltrate) tuberculosis of kidney;

II — initial destruction (papillitis or small, by diameter about 1 cm, single cavity);

III —marked destruction (caverns or policavernosial tuberculosis one of kidney segments);

IV — total or subtotal destruction (policavernose tuberculosis of two segments, tubercular pyonephrosis, calcification kidney).

They distinguish three forms of tuberculosis: tuberculoinfiltrative, ulcerous and scar.

 

Classification

 

 

 

Diagnosis of Genitourinary Tuberculosis

 

Tuberculosis of the genitourinary tract should be considered in the presence of any of the following situations:

Chronic cystitis that refuses to respond to adequate therapy,

The finding of pus without bacteria in a methylene blue stain or culture of the urinary sediment,

Gross or microscopic hematuria,

A nontender, enlarged epididymis with a beaded or thickened vas,

a chronic draining scrotal sinus,

Induration or nodulation of the prostate and thickening of one or both seminal vesicles (especially in a young man). A history of present or past tuberculosis elsewhere in the body should cause the physician to suspect tuberculosis in the genitourinary tract when signs or symptoms are present.

The diagnosis rests on the demonstration of tubercle bacilli in the urine by culture. The extent of the infection is determined by:

The palpable findings in the epididymides, vasa deferentia, prostate, and seminal vesicles,

The renal and ureteral lesions as revealed by excretory urograms;

Involvement of the bladder as seen through the cystoscope

The degree of renal damage as measured by loss of function,

The presence of tubercle bacilli in one or both kidneys.

 

 

 

 

 

 

 

 

 

 

Differential Diagnosis

               

   

Chronic nonspecific cystitis or pyelonephritis may mimic tuberculosis perfectly, especially since 15—20% of cases of tuberculosis are secondarily in­vaded by pyogenic organisms. If nonspecific infec­tions do not respond to adequate therapy, a search for tubercle bacilli should be made. Painless epididymitis points to tuberculosis. Cystoscopic demonstration of tubercles and ulceration of the bladder wall means tuberculosis. Urograms are usually definitive.

Acute or chronic nonspecific epididymitis may be confused with tuberculosis, since the onset of tuber­culosis is occasionally quite painful. It is rare to have palpatory changes in the seminal vesicles with nonspecific epididymitis, but these are almost routine findings in tuberculosis of the epididymis. The pres­ence of tubercle bacilli on a culture of the urine is diagnostic. On occasion, only the pathologist can make the diagnosis by microscopic study of the surgi­cally removed epididymis.

Amicrobic cystitis usually has an acute onset and is often preceded by a urethral discharge. "Sterile" pyuria is found, but tubercle bacilli are absent. Cystoscopy may reveal ulcerations, but these are acute and superficial. Although urograms show mild hydroureter and even hydronephrosis, there is no ulceration of the calices as seen in renal tuberculosis.

Interstitial cystitis is typically characterized by frequency, nocturia, and suprapubic pain with vesical filling. The urine is usually free of pus. Tubercle bacilli are absent.

Multiple small renal stones or nephrocalcinosis seen by x-ray may suggest the type of calcification seen in the tuberculous kidney. In renal tuberculosis, the calcium is in the parenchyma, although secondary stones are occasionally seen.

Necrotizing papillitis, which may involve all of the calices of one or both kidneys or, rarely, a solitary calix, shows caliceal lesions (including calcifications) that simulate those of tuberculosis. Careful bacteriologic studies will fail to demonstrate tubercle bacilli.

Medullary sponge kidneys may show small calci­fications just distal to the calices. The calices, how­ever, are sharp, and no other stigmas of tuberculosis can be demonstrated.

In disseminated coccidioidomycosis, renal in­volvement may occur. The renal lesion resembles that of tuberculosis. Coccidioidal epididymitis may be confused with tu­berculous involvement.

Urinary bilharziasis is a great mimic of tuber­culosis. Both present with symptoms of cystitis and often hematuria. Vesical contraction, seen in both diseases, may lead to extreme frequency. Schistosomiasis must be suspected in endemic areas; the typical ova are found in the urine; cystoscopic and urographic findings are definitive in differential diag­nosis.

Complications

A. Renal Tuberculosis: Perinephric abscess may cause an enlarging mass in the flank. A plain film of the abdomen will show obliteration of the renal and psoas shadows. Sonograms and CT scans may be more helpful. Renal stones may develop if secondary nonspecific infection is present. Uremia is the end stage if both kidneys are involved.

B. Ureteral Tuberculosis: Scarring with stric­ture formation is one of the typical lesions of tuber­culosis and most commonly affects the juxtavesical portion of the ureter. This may cause progressive hy­dronephrosis. Complete ureteral obstruction may cause complete nonfunction of the kidney.

C. Vesical Tuberculosis: When severely dam­aged, the bladder wall becomes fibrosed and con­tracted. Stenosis of the ureters or reflux occurs, caus­ing hydronephrotic atrophy.

D. Genital Tuberculosis: The ducts of the in­volved epididymis become occluded. If this is bilat­eral, sterility results. Abscess of the epididymis may rupture into the testis, through the scrotal wall, or both, in which case the spermatogenic tubules may slough out.

 

Treatment                

           

Tuberculosis must be treated as a generalized disease. Even when it can be demonstrated only in the urogenital tract, one must assume activity elsewhere. (It is theoretically possible, however, for the primary focus to have healed spontaneously.) This means that basically the treatment is medical. Surgical excision of an infected organ, when indicated, is merely an ad­junct to overall therapy.

A. Renal Tuberculosis: A strict medical regi­men should be instituted.

The following combinations of drugs can be utilized. The choice can be governed by the results of sensitivity tests. (1) Cycloserine, aminosalicylic acid (PAS), and isoniazid (INH). (2) Cycloserine, etham-butol, and INH. (3) Rifampin, ethambutol, and INH. The latter group is probably the most efficacious. The oral dose of each is as follows: Cycloserine, 250 mg twice daily; PAS, 15 g in divided doses; INH, 300 mg; ethambutol, 1.2 g; rifampin, 600 mg. Sensitivity test­ing may indicate the use of streptomycin intramuscu­larly. Administer 1 g/d the first month, 1 g 3 times a week for the next month, and then 1 g twice a week. Since INH may cause peripheral neuropathy, give pyridoxine, 100 mg/d orally. Wechsler and Lattimer (1975) prefer the combination of INH, ethambutol, and Cycloserine.

While most authorities advise appropriate medi­cation for 2 years (or longer if cultures remain posi­tive), Gow (1979) finds that a 6-month course of drugs is adequate. He recommends 600 mg of rifampin, 300 mg of INH, 1 g of pyrazinamide, and 1 g of vitamin C daily for 2 months, followed by 900 mg of rifampin, 1.5 g of pyrazinamide, and 1 g of vitamin C twice a week for 4 months.

If, after 3 months, cultures are still positive and gross involvement of the affected kidney is radiologi-cally evident, nephrectomy should be considered. Gow (1979) recommends that nonfunctioning kidneys be removed after 1-2 months of medical therapy.

If bacteriologic and radiographic studies demon­strate bilateral disease, only medical treatment can be considered. The only exceptions are (1) severe sepsis, pain, or bleeding from one kidney (may require ne­phrectomy as a palliative or lifesaving measure); and (2) marked advance of the disease on one side and minimal damage on the other (consider removal of the badly damaged organ).

B. Vesical Tuberculosis: Tuberculosis of the bladder is always secondary to renal or prostatic tuber­culosis; it tends to heal promptly when definitive treatment for the ' 'primary'' genitourinary infection is given. Vesical ulcers that fail to respond to this regi­men may require transurethral electrocoagulation. Vesical instillations of 0.2% monoxychlorosene (Clorpactin) may also stimulate healing.

Should extreme contracture of the bladder de­velop, it may be necessary to divert the urine from the bladder or perform subtotal cystectomy and anas­tomose a patch of ileum or sigmoid to the remainder (ileocystoplasty, sigmoidocystoplasty) in order to afford comfort.

C. Tuberculosis of the Epididymis: This is never an isolated lesion; the prostate is always in­volved and usually the kidney as well. Only rarely does the epididymal infection break through into the testis. Treatment is medical. If after months of treatment an abscess or a draining sinus exists, epididymectomy is indicated.

D. Tuberculosis of the Prostate and Seminal Vesicles: Although a few urologists advocate removal of the entire prostate and the vesicles when they be­come involved by tuberculosis, the majority opinion is that only medical therapy is indicated. Control can be checked by culture of the semen for tubercle bacilli.

E. General Measures for All Types: Optimal nutrition is no less important in treating tuberculosis of the genitourinary tract than in the treatment of tuber­culosis elsewhere. Bladder sedatives may be given for the irritable bladder.

F. Treatment of Other Complications: Perinephric abscess usually occurs when the kidney is destroyed, but this is rare. The abscess must be drained, and nephrectomy should be done either then or later to prevent development of a chronic draining sinus.

 

    Nephrectomy

 

 

 

 

 

                                                          Ureteroneocystostomy by Boary

 

Prolonged antimicrobial therapy is indicated. If ureteral stricture develops on the involved side, ureteral dilatations offer a better than 50% chance of cure. The severely involved bladder may cause incompetence of the ureterovesical junction on the uninvolved side. Ureteroneocystostomy cannot be done in such a blad­der; some form of urinary diversion may be required. For this reason, serial excretory urograms are neces­sary even under medical treatment.

Prognosis

The prognosis varies with the extent of the disease and the organs involved, but the overall control rate is 98% at 5 years. The urine must be studied bacteriologically every 6 months during treatment and then every year for 10 years. Re­lapse will indicate the need for reinstitution of treat­ment. Nephrectomy is rarely necessary. In the healing process, ureteral stenosis or vesical contraction may develop. Appropriate surgical intervention may be necessary.

 

 

References:

a) basic literature:

1. Donald R. Smith, M.D. General Urology, 11-th edition, 1984 p.177-244

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. Infection diseases of genitourinary tract. Editors J. Lorens, J. Dembowski, R. Zdrojowy /Dolnoslaskie wydawnictwo edukacyyne, Wroclaw 2005, p.7-50

5. Scientific Foundations of Urology. Third Edition 1990. Edited by Geoffrey D. Chisholm and William R. Fair, MD. Heinemann Medical Books, Oxford, p.123-152

b) supplementary literature:

1. Urinary Tract Infection and Inflamation / Jackson E. Fowler, JR. MD. Year Book Medical Publishers, Chicago 1989, p.138-165

       2. European Urology Supplements /2002-2007/.

       3. European Urology via www.eropeanurology.com

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

References of Tuberculosis:

1. Treatment of Tuberculosis: Guidelines for National Programmes, 3rd ed. WHO, Geneva, 2003 (http://www.who.int/docstore/gtb/publications/ ttgnp/pdf/2003.313.pdf).

2. Fain O, Lortholary O, Lascaux VV, Amoura II, Babinet P, Beaudreuil J, et al. Extrapulmonary tuberculosis in the northeastern suburbs of Paris: 141 cases. Eur J Intern Med 2000;11:145–50.

3. Warren D, Johnson JR, JohnsonCW, Franklin C. Lowe: Genitourinary TuberculosisCampbell’s Urology. 8th ed. Saunders; 2002.

4. Chattopadhyay A, Bhatnagar V, Agarwala S, Mitra DK. Genitourinary tuberculosis in pediatric surgical practice. J Pediatr Surg 1997; 32:1283–6.

5. Chuang FR, Lee CH, Wang IK, Chen JB, Wu MS. Extrapulmonary tuberculosis in chronic hemodialysis patients. Ren Fail 2003;25:739–46.

6. Ferrie BG, Rundle JS. Genitourinary tuberculosis in patients under twenty-five years of age. Urology 1985;25:576–8.

7. Queipo JA, Broseta E, Santos M, Sanchez-Plumed J, Budia A, Jimenez-Cruz F. Mycobacterial infection in a series of 1261 renal transplant recipients. Clin Microbiol Infect 2003;9:518–25.

8. Lenk S, Schroeder J. Genitourinary tuberculosis. Curr Opin Urol 2001;11:93–8.

9. Hemal AK, Gupta NP, Rajeev TP, Kumar R, Dar L, Seth P. Polymerase chain reaction in clinically suspected genitourinary tuberculosis: comparison with intravenous urography, bladder biopsy, and urine acid fast bacilli culture. Urology 2000;56:570–4.

10. Missirliu A, Gasman D, Vogt B, Poveda JD, Abbou CC, Chopin D. Genitourinary tuberculosis: rapid diagnosis using the polymerase chain reaction. Eur Urol 1996;30:523–4.

11. Moussa OM, Eraky I, El-Far MA, Osman HG, Ghoneim MA. Rapid diagnosis of genitourinary tuberculosis by polymerase chain reaction and non-radioactive DNA hybridisation. J Urol 2000;164(2):584–8.

12. Fischetti G, Lombardo G, Barrese F, Moello P, Cuzari S, Cristini C. Tb Test in the diagnosis of ‘‘closed’’ tuberculosis of the urinary tract. Minerva Urol Nefrol 1999;51(4):197–201.

13. Gow JG. Tuberculosis: genitourinary tuberculosis. Br J Hosp Med 1979;22:556–68.

14. Kao SC, Fang JT, Tsai CJ, Chen KS, Huang CC. Urinary tract tuberculosis: a 10-year experience. Changgeng Yi Xue Za Zhi 1996;19(1):1–9.

15. Flechner SM, Gow JG. Role of nephrectomy in the treatment of on functioning or very poorly functioning unilateral tuberculous kidney. J Urol 1980;123:822–5.

16. The medical Letter: Drugs for tuberculosis. Treatment Guidelines from the Medical Letter 2004;28:83-88.

17. Wise GJ, Marella VK: Genitourinary manifestations of tuberculosis. Urol Clin. North Am 2003;30:111-121.