Table of Contents  

Venyo, Venyo, Maloney, and Khan: Tuberculosis of the kidney and the genitourinary tract – a review of the literature


The World Health Organization (WHO) estimates that 9 million new cases of tuberculosis (TB) are diagnosed each year, causing over 2 million deaths annually.1 Genitourinary TB (GUTB) is the second most common type after pulmonary TB. Renal involvement remains indolent, and may not become apparent until 20 years or more following primary TB. GUTB is associated with a unilateral non-functioning kidney in 27% of cases; with renal failure in 7%.2 A recent study from India revealed that GUTB accounts for 4% of chronic renal disease and the tuberculin skin test is negative in patients with GUTB.3 The mycobacterium that causes human TB has existed for 15 000–20 000 years.4 At present, it is estimated that one-third of the world’s population is infected with this organism.4 There has been a dramatic resurgence of TB with the appearance of human immunodeficiency virus (HIV) infection/acquired immune deficiency syndrome (AIDS).4,5 Among infectious diseases, TB remains the second leading killer worldwide, with 1.5 million TB-related deaths in 2010,5,6 and it is second only to HIV infection as a cause of death from infection with a single microorganism.5,7 TB occurs in all parts of the world and eradication remains elusive.5,8 TB may result in renal dysfunction via a range of mechanisms, which include direct infection of the kidney and lower urinary tract, tubulointerstitial nephritis, glomerulonephritis, secondary amyloidosis and obstructive uropathy. Some of the associated adverse effects include mild hyponatraemia emanating from the syndrome of inappropriate antidiuretic hormone (ADH) secretion (SIADH) induced by pulmonary involvement, and nephrotoxicity caused by antituberculous agents.9 The literature reviewed below is divided into two parts: (1) overview and (2) narrations and discussions from some reported cases in the literature.


Various internet databases were used to obtain case reports and review documents on GUTB, including PubMed, Google, MEDLINE, Educus and Google Scholar. The search words used included: ‘Tuberculosis of the kidney’, ‘Renal tuberculosis’ and ‘Tuberculosis of the Genito-urinary tract’.

Results/literature review

Overview of tuberculosis of the kidney

Every year, about 9 million new cases of TB are diagnosed, and about 1.5 million annual deaths related to TB are recorded.10 The genitourinary system is the second most common site of TB infection after the lungs.11

Clinical features

Affliction of the kidney in TB may initially be symptomless, and the disease may not recognized until more than 20 years later, following the diagnosis of the of primary infection.2,11 GUTB is associated with unilateral non-functioning kidney in 27% of cases, and with renal failure in 7%.2 A recent study from India reported that the incidence of GUTB in chronic renal disease was 4%, and the tuberculin skin test was negative.3 According to Figueiredo et al.,12 in immunocompromised subjects GUTB usually causes systemic symptoms and is associated with dissemination with multiple renal foci.

Laboratory findings

Gross inspection of the tuberculous kidney usually reveals multiple cavities filled with yellow friable necrotic material.11 Figure 1a shows the macroscopic appearance of a tuberculous kidney. Microscopy may reveal caseous necrosis, with occasional granulomas, composed of epithelioid cells and Langhans giant cells with surrounding lymphocyte infiltration. Early granulomas might not show caseation. Most acid-fast bacilli (AFB) are found at the interface of viable cells and caseous necrosis.11 The microscopic features of a tuberculous kidney are show in Figure 1bf.


(a) Appearance of renal TB. Macroscopic appearance of sliced kidney with advanced TB showing severe cortical thinning and evidence of dilatation of the calyceal system. There is destruction of the renal pelvis and medulla with widespread necrotic creamy-yellow soft cheese-like material. Reported on by Dr Maloney. Reprinted with permission from Sangle N. Kidney non-tumor – infections/parasites – tuberculosis. Pathology Outlines; 2013. URL: (b) Microscopic image of TB. This shows inflamed and fibrotic renal parenchyma (left) with a few residual dilated lobules showing thyroidization. Caseating necrosis, amorphous pink featureless material (right), is also present. Reported on by Dr Maloney. Reprinted with permission from Sangle N. Kidney non-tumor – infections/parasites – tuberculosis. Pathology Outlines; 2013. URL: (c) Tuberculosis of the kidney showing caseating granulith palisading histiocytes and epithelioid cells with a peripheral rim of lymphocytes. Reported on by Dr Maloney. Reprinted with permission from Sangle N. Kidney non-tumor – infections/parasites – tuberculosis. Pathology Outlines; 2013. URL: (d) Tuberculosis of the kidney showing granulomatous inflammation; a granuloma with central caseating necrosis with a peripheral rim of inflammatory cells. A multinucleated giant cell, probably of Langhans type, is evident (lower right). Reported on by Dr Maloney. Reprinted with permission from Sangle N. Kidney non-tumor – infections/parasites – tuberculosis. Pathology Outlines; 2013. URL: (e) Tuberculosis of the kidney showing non-caseating epithelioid granulomas – early stages of TB but this is also seen in miliary TB. Reported on by Dr Maloney. Reprinted with permission from Sangle N. Kidney non-tumor – infections/parasites – tuberculosis. Pathology Outlines; 2013. URL: (f) Tuberculosis of the kidney showing non-caseating epithelioid granuloma. This can be seen in miliary TB (similar to Figure 1e). Reported on by Dr Maloney. Reprinted with permission from Sangle N. Kidney non-tumor – infections/parasites – tuberculosis. Pathology Outlines; 2013. URL:


Differential diagnosis

The differential diagnoses of tuberculous kidney includes xanthogranulomatous pyelonephritis, which has a different clinical picture and is AFB negative, although AFB may be difficult to detect even in tuberculous kidney. TB polymerase chain reaction (PCR) and AcuProbe are more sensitive.13 Occasionally fungal infections and sarcoidosis can cause non-caseating epithelioid cell granulomas.11

Miscellaneous narrations and discussions from some reported cases

De Olivera et al.14 reported the case of a 20-year-old man who presented with fever, chills, dry cough, right flank pain and oliguria. On clinical examination, a palpable mass was found in his right flank. The laboratory results were as follows: creatinine clearance was 59 ml/min/1.73 m2, tuberculin skin test was 8 mm, HIV serology was negative and urinalysis revealed sterile pyuria, but urine microscopy showed AFB. Imaging showed a fibrocavity infiltrated with small nodules in the right upper lung on a chest radiograph. Magnetic resonance imaging of the abdomen and pelvis showed significant dilatation of the right pyelocalyceal system and proximal ureter, in which there was a thickening of the middle third of the ureter and amorphous retroperitoneal structures in the perianal space with maximum measurements of 2.5 cm × 8.5 cm, which were adjudged to be consistent with grouped lymph nodes.

Biopsies of the renal cortex and retroperitoneal lymph nodes were taken and histological examination revealed caseous granulomas consistent with TB. The patient was treated with rifampicin, isoniazid, pyrazinamide (Zinamide®, Genus Pharmaceuticals, Huddersfield, UK) and ethambutol. He was left with chronic renal disease and his serum creatinine after antituberculous treatment was 61 ml/min/1.73 m2.

According to De Olivera et al.,14 (1) extrapulmonary TB accounts for about 15–20% of cases of TB in immunocompetent patients; (2) the genitourinary system is a commonly affected site; (3) GUTB often results from haematogenous spread from the primary site in the lung;15 (4) sterile pyuria is particularly suspicious of GUTB;16,17 and (5) renal dysfunction may a sequel of direct infection of the kidney parenchyma or from ureteric obstruction with resultant hydronephrosis.

Lima et al.18 reported the case of a 33-year-old man presenting with fatigue, anorexia, nausea and vomiting, progressive dyspnoea at rest, orthopnoea, paroxysmal nocturnal dyspnoea and leg oedema over the previous 2 months. In addition, the patient had a 3-year history of mild to moderate chronic flank pain radiating to the groin. He described a history of pulmonary TB, treated over a 6-month period 2.5 years before his admission, and a history of weight loss. Physical examination revealed that the patient was pale with tachypnoea and his blood pressure was 160/100 mmHg. He had a pancardiac systolic murmur and diffuse crackles on auscultation in both hemithoraces. Oedema of the legs was noted. Laboratory results showed negative serology for hepatitis B core antibodies, hepatitis B virus surface antigen, hepatitis C virus antibodies, Treponema pallidum (the causative agent of syphilis) and HIV antibodies. Other laboratory results included haemoglobin 4.6 g/dl, haematocrit 14.5%, white blood count 1140/mm3, platelets 261 000/mm3, blood urea nitrogen 273 mg/dl, creatinine 13.6 mg/dl, bicarbonate 21 mEq/l (reference range 24–26 mEq/l), sodium 138 mEq/l (normal 135–145), potassium 5.5 mEq/l (normal 3.5–5.0 mEq/l), total calcium 7.1 mg/dl (normal 8.4–9.5 mg/dl), phosphorus 11.4 mEq/l (reference range 2.5–4.5 mEq/l) and parathyroid hormone 1715 pg/ml (normal 150–300 pg/ml).

The patient also had oliguria of 400 ml/24 hours and underwent haemodialysis. His anaemia was determined to be a consequence of his chronic kidney disease. Investigations for ferropenic anaemia and other anaemias were negative. He had a blood transfusion and was given erythropoietin. The urinalysis showed: pH 6.0, leucocytes 1+, protein 4+, erythrocytes 3+, uncountable leucocitary casts and negative urine culture. An ultrasound scan showed a small right kidney that measured 7.5 cm × 4.5 cm × 5.8 cm (the left kidney measured 12 cm × 5.8 cm × 5.8 cm), bilateral nephrolithiasis, left hydronephrosis with reduction of parenchyma and complex cyst in the right kidney with peripheral calcifications. The patient also underwent computerized tomography (CT) of the abdomen and thorax, which revealed features adjudged to be compatible with TB. With a presumed diagnosis of disseminated TB, the patient underwent a cutaneous tuberculin test, which measured 17 mm. He also gave 10 samples of urine for mycobacterial culture and underwent bronchoscopy with culture for Koch bacilli from the bronchoalveolar lavage and thoracocentesis with pleural biopsy. All the mycobacterial cultures were negative. At follow-up, renal and pleural extrapulmonary TB were considered the main possible diagnoses. The authors stated that Light’s criterion of the pleural fluid was compatible with exudate and adenosine deaminase of 50 U/l, and empirical treatment was commenced with tuberculostatic agents, which were adjusted according to the Brazilian guidelines for TB. The patient became stable and he was discharged. At that time he was asymptomatic but without recovery of renal function, which was treated with haemodialysis three times a week.

Sallami et al.19 reported on a 53-year-old man who presented with pain in the right flank and weight loss over the course of 7 months but was otherwise asymptomatic. He had no history of fatigue, loss of appetite, fever, chills or respiratory symptoms. He denied any history of exposure to TB. He was otherwise in good health and had no history of diabetes mellitus, hypertension or other medical problems. Physical examination revealed right flank tenderness but no palpable mass. A renal ultrasound showed a heterogenic and hypoechoic mass at the lower pole of the right kidney, measuring 6 cm × 8 cm with fine calcifications. Intravenous pyelography confirmed a lower pole tumoral syndrome (deformities and compression of low calyceal cavities). CT revealed a cystic renal mass with enhancing multiple thin and regular septa with no calcifications. Radiography of the chest was normal. A basic haematological workup was unremarkable except for mild anaemia. The patient underwent a partial right lower pole nephrectomy. Histological examination of the specimen was consistent with renal TB. He was treated with antituberculous therapy for 8 months. He remained in good health after 120 months of follow-up.

Colbert et al.20 made the following statements:

  • HIV is the most common cause of infectious disease-related deaths, followed by TB.21

  • WHO data indicate that one-third of the world population has been exposed to TB and has at least latent TB.10

  • The global total of 9.4 million cases of active TB has been documented, with an incidence of active TB ranging from 30 to 340 cases (mean 140) per 100 000 people.

  • With regard to the global prevalence of active TB, 14 million cases have been documented and the prevalence of active TB ranges between 40 and 500 cases per 100 000 people, with a mean prevalence of 165 per 100 000 people.

  • Annual TB-associated mortality ranges between 2 and 50 per 100 000 people; and mean TB-related mortality is 19 per 100 000 people, with a total annual death rate of 1.3 million.

  • In the USA, TB often afflicts patients with malignancy, immunosuppression or HIV infection.

  • The causative microorganism of TB is Mycobacterium tuberculosis, which tends to be inhaled into the lung, where the bacteria are locally contained by leucocytes and macrophages. Some organisms will cause active pulmonary disease and other organisms will spread to distant locations as metastatic foci.

  • Extrapulmonary TB occurs in only 20% of cases.16

  • The lymph node is the most common site of extrapulmonary TB infection, while GUTB is the second most common site of extrapulmonary TB infection. GUTB has been reported to account for 15–30% for all cases of extrapulmonary TB.2227

  • It had been suggested that renal TB occurs via haematogenous spread of previously dormant organisms from a previous lung infection at the time of marginal cellular immunity.28 The organisms need strict growth requirements. The fact that the kidney has a high oxygen tension makes it a prime site for new growth.

  • The initial manifestation in the kidney is the presence of multiple cortical granulomas.

  • As a sequel of impairment of the defences of the host, the granulomas tend to grow, coalesce and eventually result in caseous necrosis.

  • The response of the kidney to the now active infection leads to an intense interstitial nephritis with severe calcifications.

  • TB of the kidney does not usually manifest with the classical symptoms of fever, weight loss or night sweats.

  • Radiological imaging of the kidney will usually alert a clinician to the suspicion of GUTB.29

  • Cystoscopy and retrograde ureteropyelography may reveal a markedly abnormal urinary bladder and classical changes of ureteritis cystica.

  • A definitive diagnosis of GUTB can be established by the isolation of the TB organisms from the urine or tissue biopsy specimens. Furthermore, microscopic examination of centrifuged urine may show AFB.

  • Histological examination of renal TB tends to show tubule interstitial nephritis with granuloma formation, quite often with caseous necrosis.16,30

  • A number of authors3133 consider urine culture for AFB to be the gold standard for establishing the diagnosis of renal TB; its specificity is 100%, but its sensitivity ranges between 30% and 90% depending on the number of samples that have been tested, and it may take 6–8 weeks before a positive urine culture may become available.

  • With regard to TB of the kidney, the renal outcomes tend to be very variable. Diffuse renal scarring may result in autonephrectomy in which and the affected kidney becomes functionless.

  • The spread of intrarenal infection to the renal pelvis could emanate in pyonephrosis with a ‘cement’ or ‘putty’ kidney, which tends to involve the entire renal pelvis.

  • Progression to end-stage kidney disease in patients with renal TB is very unusual.

  • The treatment of TB of the kidney entails the use of multidrug therapy, which has evolved to the current four-drug therapeutic regimen. This involves an initial 2-month intensive treatment with rifampicin (rifampin), isoniazid, pyrazinamide and ethambutol,16,34 followed by a 4-month maintenance therapeutic regimen with rifampicin (rifamoin) and isoniazid.

  • Urological intervention may be necessary for unilateral disease because of pain or haemorrhage or augmentation of the urinary bladder.35,36

  • Relief of unilateral ureteric obstruction by means of ureteric stenting or insertion of percutaneous nephrostomy might be necessary, particularly if the underlying kidney parenchymal disease is mild, and the residual renal function has an estimated glomerular filtration rate > 15 ml/min, in which escape from dialysis might occur.



AFB-positive rates among single urine specimens from patients with active disease are reported to range from 11% to 80%, depending upon the demographic group and stage of infection.37,38 Therefore, Pais et al.9 recommended that three to six early morning midstream specimens of urine should be obtained to culture AFB to maximize positivity in GUTB.

The demonstration of AFB in the urine sediment by means of Ziehl–Neelsen stain or fluorescent dye is not diagnostic, as non-pathogenic mycobacteria show similar staining.39 False-negative results may occur in the setting of concomitant antituberculous or antibacterial therapy, which is capable of inhibiting mycobacterial growth (particularly if fluoroquinolones are used).39 The use of PCR for detection of M. tuberculosis in urine or renal tissue improves diagnostic yield; sensitivity and specificity range from 87% to 100% and from 93% to 98%, respectively.37,40,41

Imaging studies

Figures 2af, 3af, 4af and 5af show various radiological investigations that illustrate various aspects of GUTB encountered by the coauthor Dr Ali Nawaz Khan.


(a) Renal TB-lymphatic fistula. (b) Renal TB-lymphatic fistula. (c) Renal TB-lymphatic fistula. (d) Plain radiograph of the abdomen in a woman with renal TB shows calcification of varying patterns (curvilinear, amorphous and speckled). (e) Excretory urography in a patient with renal TB shows an irregular cavity at the upper pole calyx of the right kidney. Note the multiple tiny calcifications in the liver, spleen and right adrenal gland because of calcified tuberculous granuloma. (f) Excretory urography in a patient with renal TB shows multiple curvilinear calcifications in the left kidney. Note the calyceal dilatation in the upper pole of the left kidney because of infundibular stricture. Images courtesy of Dr Khan.


(a) Excretory urography in a man with renal TB shows irregular cavitation of the left upper pole calyx. Note the multiple tiny calcifications in the spleen. (b) Intravenous urography series in a man with renal TB shows marked irregularity of the bladder lumen because of mucosal oedema and ulceration. (c) Excretory urography in a woman with a history of TB of the breast. The film shows irregular cavitation in the lower pole calyx of the left kidney because of renal TB. (d) Excretory urography in a patient with advanced renal TB shows lobar calcification (mainly right) with no excretion of contrast on intravenous urogram. (e) Excretory urography in a patient with TB of the ureter and bladder. The lower end of the right ureter demonstrates an irregular calibre with an irregular stricture at the right vesicoureteric junction. Note the asymmetrical contraction of the urinary bladder, with marked irregularity because of oedema and ulceration. (f) Plain radiograph of the abdomen in a patient with calcified seminal vesicles because of TB. Note the amorphous and speckled calcification in the right kidney. Images courtesy of Dr Khan.


(a) Lateral view of the abdomen in a patient with schistosomiasis shows tubular calcification of the ureters in contrast to the speckled calcification in TB. (b) Radiograph of the pelvis in a patient with schistosomiasis shows fine linear calcifications of the bladder wall with normal volume. In TB, the bladder is contracted and demonstrates speckled calcification. (c) Hysterosalpingogram in a patient with TB of the uterus. The contour of the uterus is irregular, with nodular filling defects. (d) Hysterosalpingogram in a patient with TB of the fallopian tubes shows right-sided hydrosalpinx with an occluded left fallopian tube. (e) Ultrasound image of the pelvis shows left tubo-ovarian abscess resulting from TB. (f) Ultrasonography image of the scrotum in a young male patient shows left epididymo-orchitis resulting from TB. Images courtesy of Dr Khan.


(a) Renal TB causing psoas abscess. (b) Renal TB causing psoas abscess. (c) TB peritonitis secondary to TB of the uterus. Images (a) to (c) courtesy of Dr Khan. (d) TB stricture lower ureter. Image courtesy of Dr Ravi Kadasne. (e) Ultrasound TB RENAL ABSCESS. Image courtesy of Dr Durr-e-Sabih, Director, Multan Institute of Nuclear Medicine and Radiotherapy Multan – Pakistan. (f) TB epididymo-orchitis. Image courtesy of Dr Khan.


Intravenous urography

A diagnosis of GUTB Is indicated by involvement of the both upper and lower urinary tract on intravenous pyelography (IVP); involvement of only the upper urinary tract is insufficient.42 Scout films or plain radiographs may show calcifications. IVP is used for the evaluation of suspected renal TB in settings where other modalities are not available. IVP may be normal in early disease, but, by the time symptoms develop, moderate to marked urinary tract abnormalities are usually present. The earliest reported findings include (1) erosion of the tips of the calyces, (2) narrowing of collecting system infundibula, (3) blunting of the calyces or (4) overt papillary necrosis with associated parenchymal scarring and calcification.42,43,45 These findings may be unilateral or bilateral and may resemble those seen in chronic pyelonephritis or papillary necrosis of other causes. Reported signs of extrarenal disease include single or multiple ureteral strictures, a contracted bladder and, in males, calcifications in the vas deferens, seminal vesicles or prostate.42,44

Computerized tomography

Computerized tomography reveals asymmetrical caliectasis, hydronephrosis and/or ureteral stricture. Asymmetrical caliectasis reflects uneven infundibular scarring. Caliectasis accompanied by thickened and/or enhancing walls and calcification can mimic the appearance of complex renal cysts.45 CT shows periureteral and perirenal fibrosis, which enables the delineation of pararenal sinus tracts, and allows the identification of the ‘autonephrectomy’.18,46,47

Conditions associated with renal tuberculosis

Chronic interstitial nephritis

Some case reports and retrospective studies describe an association between chronic interstitial nephritis and TB.16,30,48,49 The diagnosis of tuberculous interstitial nephritis requires three to six urine cultures for AFB, together with radiography.9 Tuberculous interstitial nephritis is unlikely in the setting of negative urine culture and the absence of TB elsewhere.9 The pathogenesis of TB-associated interstitial nephritis is not clear; it may be an immunological epiphenomenon induced by TB in other organs.50 Chapagain et al.30 reported a series of 25 patients, of Asian descent, who presented with TB and significant renal disease; chronic granulomatous interstitial nephritis was the primary lesion in all who underwent biopsy (68%). Histological examination of renal biopsy specimens revealed interstitial inflammation with eosinophilia and granulomas and, in three patients, caseating granulomas. There was no evidence of immune complex deposition in any of the samples, although non-specific mesangial IgG deposition was observed. No biopsy was positive for AFB by Ziehl–Neelsen staining or culture. Leucocyturia was the most common observation but was not a universal finding. Nine patients had systemic TB. Active urine sediment and rapidly progressive renal failure were observed in eight patients, but there were no extrarenal symptoms related to TB.

Tuberculous glomerulonephritis

Pais et al.9 describe the association of glomerulonephritis and TB. The diagnosis of tuberculous glomerulonephritis is difficult to establish, particularly during the early stages of disease, but it is an important consideration since treatment of glomerulonephritis with steroids can worsen underlying TB. In one retrospective study of 46 Chinese patients with tuberculous glomerulonephritis, 76% had a history of pulmonary or extrapulmonary TB. Most patients were symptomatic with oedema and fatigue and had haematuria (67%) and proteinuria (70%); pyuria was observed in 11% of cases. A positive urine AFB culture was observed in 20% of cases, and renal biopsy was PCR positive for TB in 85% of cases.51

Secondary amyloidosis

Secondary amyloidosis occurs in the setting of chronic inflammation, leading to high circulating levels of serum amyloid A protein. Secondary amyloid should be suspected in patients with TB who exhibit proteinuria in the nephrotic range.52,53

The diagnosis of secondary amyloidosis is established by demonstrating tissue amyloid deposition on biopsy of the abdominal fat pad, rectum or kidney.9 According to Pais et al.9, in contrast to secondary amyloidosis, primary vascular amyloidosis causes glomerular ischaemia, but it does not cause an increase in glomerular permeability. It has also been reported that the clinical manifestations in this setting include slowly progressive renal failure, a benign urine sediment and little if any proteinuria.54


Mild hyponatraemia (plasma sodium concentration between 125 and 135 mEq/l) has been described in the setting of active pulmonary or miliary TB.9,53 Most patients appear to have SIADH. A third have a reset osmostat in which the plasma sodium concentration is stable at a new lower level. The factors responsible for the persistent ADH release are not known, but hyponatraemia and abnormal water handling resolve following effective treatment of TB.53

Drug-induced nephrotoxicity

Some antituberculous drugs can affect renal function.55 Rifampin can induce tubular and interstitial injury and, in rare cases, can cause crescentic glomerulonephritis.55 Pais et al.9 describe renal failure within hours of the first dose, but it can also occur with intermittent or discontinuous long-term therapy. Patients typically present with acute renal failure with interstitial nephritis on renal biopsy. Tubular function is also abnormal and can lead to renal glycosuria, hyperuricosuria, polyuria due to nephrogenic diabetes insipidus and increased urinary excretion of polyclonal light chains, which can lead, in rare cases, to tubular obstruction, simulating myeloma kidney.56 Ethambutol and pyrazinamide are not nephrotoxins, but can cause a selective decrease in uric acid excretion because of diminished secretion or enhanced reabsorption.55,56 Hyperuricaemia may be seen in 40–50% of these patients.55 Gout occurs, but with no associated risk of acute uric acid nephropathy since uric acid excretion is not enhanced.


The approach to treatment of renal TB is the same as that for pulmonary TB.9 Standard antituberculous agents for 6 months are successful in the eradication of active renal infection for drug-susceptible TB.57 Dose adjustment of medications is needed in the setting of renal insufficiency. The treatment regimen varies depending on whether or not the patient has HIV infection or drug-resistant TB. The clinical response to antituberculous therapy is favourable in view of the high urinary concentrations of antituberculous agents and excellent renal vascular supply. The urine is rendered sterile within 2 weeks of initiating therapy. Weir and Thornton58 reported on seven patients with culture-confirmed urinary tract disease who were treated with standard therapy: no relapse was observed. Relapse rates among patients who require nephrectomy appear to be relatively low; one large study59 reported a relapse rate < 1%; however, another study of 174 patients60 found a relapse rate of 19% even after 12 months of therapy.

Pais et al.9 reported that, of 135 patients who were treated for renal TB in the 1960s with 6 months of isoniazid, streptomycin and para-aminosalicylic acid (Granupas®, Lucane Pharma, Paris, France), urine culture after 10 years of follow-up was negative in 97%; 60–90% of patients required a combination of surgical and medical therapy.61 In a follow-up study of 135 patients with renal TB who were treated with isoniazid, rifampin and ethambutol for 6–9 months (1970 to 1974) or isoniazid, rifampin and pyrazinamide for 6 months (1975 to 1977), the cure rate was 100% (measured by urine sterilization); relapse occurred in one patient.9 Psihramis and Donahoe62 recommended that patients receiving antituberculous therapy be monitored for signs/and symptoms of upper urinary tract obstruction (flank pain, renal colic, hydronephrosis) during treatment.

According to Figueiredo and Lucon,59 clinical worsening may be observed in the first few weeks of antituberculous therapy because of inflammation, followed by fibrosis and obstruction of the collecting system. Ureteral strictures may progress during the course of treatment because of scarring and subsequent narrowing of the lumen.44 In a retrospective study carried out by Shin et al.,63 of 21 kidneys that developed strictures during the course of antituberculous therapy, 76% developed within the initial 2 months of treatment. The authors also reported that early endourological decompression with ureteral stent or percutaneous nephrostomy placement was associated with a nephrectomy rate lower than treatment with medication alone (27% vs. 66%). Apart from endourological decompression, other surgical intervention for GUTB should be delayed until the patient has received at least 4 weeks of antituberculous medical therapy.35 Delayed definitive reconstruction for stricture may include ureteral reimplantation, ureteroureterostomy, pyeloplasty or ureteral substitution and should be based upon the location and length of remaining stricture.35 In the setting of non-functioning kidney and associated sequelae, including urosepsis or poorly controlled hypertension, nephrectomy should be considered.35

Renal, ureteral and bladder tuberculosis

Lessau and Kim64 made the following statements:

  • TB may affect any part of the genitourinary tract.

  • Multiple granulomata form at the site of metastatic foci; these are often bilateral, and tend to be found in cortical areas and adjacent to the glomeruli, which may remain inactive for decades.

  • Even though both kidneys are seeded, clinically significant disease, which is caused by capillary rupture and delivery of proliferating bacilli into the proximal tubules, tends to develop in only one kidney.

  • The medullary hypertonic environment tends to impair phagocytic function.

  • Growing granulomata may invade the calyceal system, following which the bacilli may disseminate to the renal pelvis, ureters, bladder and other genitourinary organs.

  • Depending upon the state of the patient’s defence mechanisms, fibrosis and strictures may develop with chronic abscess formation.

  • Extensive lesions can emanate in non-functioning kidneys.

  • Hypertension in persons with TB of the kidney is twice as common as it is in the general population.

  • TB of the ureter tends to be an extension of the disease from the kidneys, to the ureterovesical junction, and this tends to develop in about half of all patients with TB of the kidney. TB of the ureter only rarely affects the middle third of the ureter.

  • TB of the ureter quite often leads to ureteric strictures and, at times, leads to hydronephrosis.

  • Rarely, severe cases of TB of the ureter can cause stricture of virtually the entire ureter.

In addition, Lessau and Kim64 reported that:

  • TB of the urinary bladder tends to develop secondary to TB of the kidney, and this often tends to start at the ureteric orifice.

  • At the onset TB of the urinary bladder manifests as superficial inflammation with bullous oedema and granulation.

  • Fibrosis of the ureteric orifice may result in stricture formation with hydronephrosis or scarification (e.g. golf-hole appearance) as a result of vesicoureteric reflux.

  • Severe cases of TB of the urinary bladder tend to involve the entire wall of the bladder, and deep layers of the urinary bladder muscle are eventually replaced by fibrous tissue, which results in a thick fibrous bladder.

  • Tubercles are rare in the urinary bladder, but if they are present, they tend to appear at the ureteric orifice.

  • Malignancy should be taken into consideration when any isolated tubercles away from the ureteric orifices are encountered.

Tuberculosis of the epididymis and testis

With regard to TB of epididymis and testis, it has been stated that:

  • The higher frequency of isolated TB of the epididymis in children suggests haematogenous spread of infection.64

  • In adults, tuberculous epididymo-orchitis is caused by direct spread from the urinary tract.65

Lessau and Kim64 also found that:

  • The development of a draining sinus is uncommon in developed countries; nevertheless, induration of the epididymis and beading of the vas deferens tend to be common.

  • TB involvement of the testis tends to be a sequel of direct extension.

  • The development of bilateral obstruction of the vas deferens may lead to infertility.

  • Nodular beading of the vas deferens characteristically tends to be a physical finding.

  • Furthermore, the orchitis and the resulting swelling of the testes could be difficult to differentiate from other mass lesions of the testes.

Tuberculosis of the prostate gland

With regard to TB of the prostate gland, Lessau and Kim64 as well as Paick et al.66 reported:

  • TB of the prostate is also spread by the haematogenous route, but involvement of the prostate gland is rare; nevertheless, among those whose prostate glands are affected by TB, 85% also have TB of the kidney.64,66

  • TB of the prostate gland tends to be nodular and non-tender to palpation.64,66

  • Severe cases of TB of the prostate may cavitate and form a perineal sinus, although this is rare.64,66

  • In cases of TB of the prostate gland, decreased semen volume may indicate extensive prostatic disease or ejaculatory duct obstruction.64,66

Tuberculosis of the urethra and the genitals

According to, Lessau and Kim64:

  • TB of the urethra ensues secondarily to genital TB.65

  • Genital TB and TB of the urethra manifests with a superficial tuberculous ulcer on the penis or in the female genital tract as a result of exposure to mycobacteria during intercourse. The penile ulcer may lead to cavernositis which extends to the urethra.64

  • TB of the urethra and genitalia may involve the uterus and fallopian tubes, and may cause strictures.64

  • Malignancy should be considered in the presence of genital ulcers.64

  • Acute urethritis manifests as mycobacterial discharge and often results in chronic stricture formation.64


Genitourinary tract TB occurs in 4–20% of patients with pulmonary TB. Haematogenous renal seeding at the time of primary TB infection causes granulomas in proximity to glomeruli, which can caseate and rupture into the tubular lumen. Subsequently, tuberculous bacilli can enter the medullary interstitium, leading to progressive medullary injury. Destruction of renal papilla could lead to calyceal ulceration or abscess formation. Involvement of the collecting system may cause scarring and stenosis. Initially the onset of GUTB is insidious. Lower urinary tract symptoms and malaise are later occurrences. Systemic symptoms are relatively rare. Pyuria and/or microscopic haematuria are present in more than 90% of cases. Ureteral stricture may cause obstructive uropathy. The diagnosis of GUTB is established by demonstration of AFB in the urine; the constellation of dysuria, sterile pyuria, haematuria and characteristic radiographic findings is highly suggestive of the diagnosis. Three to six early-morning midstream specimens are taken to test for AFB and cultured to maximize positivity. Among patients with active renal TB, 30–40% of single urine specimens will be positive on AFB culture. PCR also provides a useful diagnostic tool with 87–100% sensitivity and 93–98% specificity. Imaging that reveals both upper and lower urinary tract changes, associated with calcifications, calyceal distortion and infundibular and ureteral strictures is more suggestive of GUTB than of other obstructive renal pathology. Other conditions associated with TB of the kidney include tubulointerstitial nephritis, glomerulonephritis, secondary amyloidosis and obstructive uropathy. Associated adverse effects of TB of the kidney include mild hyponatraemia as a result of SIADH which has been induced by pulmonary involvement and nephrotoxicity caused by antimycobacterial agents. The approach to antituberculous therapy for GUTB is similar to the treatment for pulmonary TB. Early endourological decompression of the affected kidney, which is obstructed, improves the salvage rate of the affected kidney.


Genitourinary tract TB occurs in 4–20% of patients with pulmonary TB. The initial presentation of this condition is usually insidious. Pyuria and microscopic haematuria occur in more than 90% of patients. Diagnosis is by the demonstration of tubercle bacilli in urine. Radiological findings include calcifications, calyceal distortion and infundibular and ureteral strictures, which strongly indicate the presence of GUTB. The initial findings include erosion of the tips of the calyces, narrowing of collecting system infundibula, blunting of the calyces or overt papillary necrosis with associated parenchymal scarring and calcification. Associated conditions of TB of the kidney include tubulointerstitial nephritis, glomerulonephritis, secondary amyloidosis and obstructive uropathy. TB of the prostate gland is nodular and non-tender. Genital TB and TB of the urethra manifest with a superficial tuberculous ulcer on the penis or in the female genital tract. Infertility may be a consequence of bilateral obstruction of the vas deferens. Nodular beading of the vas deferens is a characteristic physical finding, and the orchitis and the testicular swelling can be difficult to differentiate from other mass lesions of the testes. The approach to antituberculous therapy for TB of the kidney is the same as that for pulmonary TB. Early endourological decompression of the affected kidney, which is obstructed by stricture, would appear to improve the salvage rate of the kidney.


The authors acknowledge Pathology and Dr N Pernick President of Pathology for granting permission to reproduce figures from their website.



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