Wednesday, June 29, 2011

GENITO-URINARY TRACT TUBERCULOSIS



A 38 year old lady presented to us with lower urinary tract symptoms and right flank pain for 15 days.She had history of undergoing left nephrectomy in 2002.The histopathological evaluation had shown granulomatous nephritis.After the surgery; she was advsied scrupulous follow-up but she could not regularly visit the surgeon.On presentation to our hospital; she had deranged creatinine(2.7 mg%) with sonographic evidence of right moderate hydroureteronephrosis.Non contrast CT scan evaluation confirmed the sonographic findings.She was taken up for retrograde pyelography and stenting.The findings on RGP were hydroureteronephrosis with a stricture at pelvi-ureteric junction.The bladder capacity was small around 90 ml.She was subjected to bladder biopsy.



GUTB: A REVIEW
Genitourinary tuberculosis is hematogeneous infection of the kidneys. The kidney being a primary organ the rest of the organs are affected by direct extension. The disease progression depends upon the host immune response.
The urologist many a times consider the GUTB as the diagnosis of exclusion. Any longstanding lower urinary tract symptoms with obvious cause detected makes the urologist suspicious about the disease.
Recurrent UTIs, frequency, dysuria, painless hematuria, painful ejaculation, anejaculation etc are the predominant symptoms.
Pathology: Tuberculosis results in development of Caseating granulomas - Langhans giant cells surrounded by lymphocytes and fibroblasts. The course of the infection depends on the virulence of the organism and the resistance of the host.
The healing process results in fibrous tissue and calcium salts being deposited, producing the classic calcified lesion. The disease because of fibrotic/calcific nature results in development of strictures,deformed calyces,small capacity bladder(so called thimble bladder).The irony of the treatment is that the starting of the antiKochs medications results in further fibrosis.This can lead to further narrowing of the strictures and / or further decrease in bladder capacity.
We therefore usually add steroids in initial management to prevent further compromise of the renal functions.
In the present case the disease had already taken a toll of left kidney.(hematogeneous route).The rest of the disease was probably because of direct extension( small bladder capacity and multiple ureteric strictures).
The treatment in our case was –stenting to safeguard the kidney function by stenting,bladder biopsy for getting final histopathological proof.The next strategy would be starting her on AKT and steroids and keep stent for 3-6 months period.Any recurrent stricture/persistence of thimbe bladder would need specific surgery.





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