Renal tuberculosis
Renal TB occurs as a result of hematogenous spread of bacilli to the renal cortex from pulmonary lesions, either at the time of initial TB infection or due to the late breakdown of an old caseous lesion. Due to high renal blood flow some level of seeding always occurs, however in non-immunocompromised patients this is managed by effective cell-mediated immunity, in those who are immunocompromised, renal TB can develop.
Renal TB is characterised by a caseous lesions that may necrose and destroy functioning renal parenchyma. These lesions scar, and fibrose, which can lead to strictures or hydronephrosis and obstructive uropathy. Bilateral disease is frequently present, however, acute or chronic renal failure is uncommon due to the time required to the lesion to take hold. Most frequent presentation is dysuria, hematuria and abdominal/flank pain.
Cut kidney in renal tuberculosis: much of the parenchyma is replaced by white, cheese-like caseous necrosis with cavities around the calyces.
Image: “Renal tuberculosis (6539942987)” by Yale Rosen from USA, CC BY-SA 2.0, via Wikimedia Commons.
Commonly urinalysis is abnormal, with hematuria and pyuria common, cultures for M.tuberculosis are also often positive, and almost all patients are reactive to the tuberculin skin test (TST).
The mainstay of treatment of renal TB is short-course chemotherapy. In highly advanced cases partial or complete nephrectomy may be required.