Urogenital Tuberculosis (UG-TB)

Epidemiology

UG-TB is diagnosed in 1.1–1.5% of all TB cases and 5–6% of extrapulmonary TB cases. Men are infected twice as often as women. Most patients are 20–40 years of age. The average latent period from initial pulmonary infection to clinical UG-TB is 22 years (range 1–46 years). — Brenner and Rector's The Kidney

Organs affected:

Kidneys: 60–100%
Ureters: 19–41%
Bladder: 15–20%
Prostate/epididymis: 20–50% of men

Pathogenesis

Primary TB (usually pulmonary) → haematogenous dissemination → seeding of the renal cortex (favoured by high oxygen tension) → latent foci → reactivation years later (characteristically unilateral).

From the kidney, infection descends contiguously through urine to the collecting system → ureter → bladder → prostatic urethra → prostate/seminal vesicles → epididymis. The prostate can also be seeded directly haematogenously.

Pathogenesis of TB of the urinary tract showing route of infection descending from kidney through bladder to prostate and epididymis

Pathogenesis of urogenital TB — Smith and Tanagho's General Urology

Pathology by Site

Kidney & Ureter

The initial cortical granulomas caseate and liquefy → cavitation. Pus discharges into the calyx → calyceal erosion → papillary necrosis → progressive destruction. The kidney surface may appear grossly normal early, but on section shows cheesy caseation. The ureter becomes fibrosed and shortened, producing a "golf-hole" (gaping) ureteral orifice — a sign of an incompetent vesicoureteric junction.

In advanced disease the entire kidney is replaced by caseous material. Calcium deposition during repair causes autonephrectomy (a fibrosed, functionless kidney with or without calcification). This occurs in 23–33% of cases; 27% of patients worldwide present with a non-functioning unilateral kidney. — Brenner and Rector's The Kidney

Microscopy: the classic triad — caseating necrosis + epithelioid histiocytes + Langhans giant cells.

Bladder

Infected urine bathes the mucosa → tubercles form (especially near the involved ureteral orifice) → coalescence → ulceration (may bleed) → fibrosis → "thimble bladder" (small-capacity contracted bladder) → marked urinary frequency. Ureteral reflux or stenosis may cause hydronephrosis. — Smith and Tanagho's General Urology

Prostate & Seminal Vesicles

Infected urine traversing the prostatic urethra seeds the prostate. Tuberculous granulomatous prostatitis can elevate PSA and mimic prostate carcinoma clinically.

Epididymis & Testis

Extension along the vas or perivasal lymphatics from the prostate. Usually painless (chronic indolent course). Extensive abscess may rupture through the scrotal skin creating a permanent sinus.

Clinical Features

Up to 50% of patients have no localising genitourinary symptoms. Presentations include:

Category	Features
Asymptomatic	Incidental finding; "sterile pyuria"
Urinary	Dysuria, frequency, haematuria, flank pain
Systemic	Fever, weight loss, night sweats (25–33%)
Male genital	Hard non-tender epididymis, beaded vas deferens, nodular prostate, nontender testicular mass
Female genital	Infertility, pelvic pain

The classic clue: "sterile (acid) pyuria" — pyuria with negative routine bacterial cultures, acidic pH urine. UG-TB should be suspected when conventional antibiotics fail for apparent UTI. — Comprehensive Clinical Nephrology

Diagnosis

Urine Examination

Urinalysis: abnormal in >90%; most common finding is sterile pyuria + haematuria
At least 3 (preferably 5) consecutive early-morning urine cultures for M. tuberculosis — sensitivity 65%, specificity 100%; takes 6–12 weeks (conventional) or ~2 weeks (MGIT liquid culture — WHO gold standard)

Molecular Tests

GeneXpert MTB/RIF (PCR): sensitivity ~95%, specificity ~90%; simultaneously detects rifampicin resistance; can be used on urine. Note: may give false positives post-treatment due to residual DNA.
Xpert XDR: also detects resistance to isoniazid, injectable agents, fluoroquinolones

Immunological

IGRA (QuantiFERON TB Gold / T-SPOT): sensitivity and specificity >90%; not affected by prior BCG vaccination; identifies latent or active disease — preferred over TST
TST/Mantoux: positive in 60–90% of cases; affected by BCG vaccination; now rarely used

Histopathology

Pathologic triad: caseating necrosis + epithelioid histiocytes + Langhans giant cells
Ultrasound-guided FNA/biopsy of renal lesion useful
Endoscopy (cystourethroscopy, ureteroscopy, hysteroscopy, laparoscopy) for anatomic assessment and biopsy

Imaging

CT is now preferred over IVP. Characteristic findings (roughly in progression):

Calyceal erosions (earliest)
Papillary necrosis
Renal parenchymal cavitation, dilated calyces, hydronephrosis
Ureteral wall thickening + strictures (most common in distal third)
Bladder wall thickening, reduced volume, filling defects
Calcification patterns (curvilinear, amorphous/speckled, ureteric)
Autonephrectomy (densely calcified, non-functioning kidney)

Management

Medical (First-Line Anti-TB Therapy)

The standard regimen follows general TB treatment principles:

2 months HRZE (isoniazid + rifampicin + pyrazinamide + ethambutol) induction
4 months HR (isoniazid + rifampicin) continuation = 6 months total for drug-sensitive disease

Corticosteroids are used adjunctively for ureteric strictures and bladder involvement to reduce fibrosis.

Surgical

Indications include: obstructive complications (ureteral stricture, hydronephrosis), non-functioning kidney, contracted bladder, or diagnostic uncertainty. Procedures include:

Nephrectomy/nephroureterectomy for autonephrectomy or severely damaged kidney
Ureteral reconstruction / reimplantation for strictures
Augmentation cystoplasty for contracted (thimble) bladder
JJ stenting or nephrostomy for acute obstruction

Surgery is almost always performed after or alongside anti-TB chemotherapy, not instead of it. — Comprehensive Clinical Nephrology

Key Complications

Autonephrectomy (23–33%)
Renal failure (1–10%)
Ureteral stricture → hydronephrosis
Thimble bladder (severe frequency/urgency)
Male infertility (epididymal/vasal damage)
Female infertility (fallopian tube involvement)

Sources: Comprehensive Clinical Nephrology, 7th Edition | Brenner and Rector's The Kidney | Smith and Tanagho's General Urology, 19th Edition

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