Current concepts on pathogenesis of renal tuberculosis.
The pathogenesis of renal tuberculosis begins with the initial localization of the tubercle bacilli in the cortical glomeruli causing mechanical stress which lead to alteration in cell morphology, increased rate of protein synthesis and proliferation of resident glomerular cells as well as the infiltrating blood borne cells. The infection may remain localized to the renal parenchyma resulting in various forms of glomerulonephritides and/or gain access to the calyceal system causing pyelocalyceal destruction with subsequent ureteric and urinary bladder involvement. The disease may remain quiesent at the foregoing stage or progress to hydronephrosis and pyonephrosis as a result strictures and obstruction. This communication discusses the immunological responses and various specific lesions resulting from renal injury caused by mycobacterium tuberculosis.
Chijioke
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Renal Unit, Department of Medicine, University of Ilorin Teaching Hospital.
D000686:Amyloidosis / Q000382:microbiology; D002908:Chronic Disease; D018450:Disease Progression; D005921:Glomerulonephritis / Q000382:microbiology; D006801:Humans; D006869:Hydronephrosis / Q000382:microbiology; D009395:Nephritis, Interstitial / Q000382:microbiology; D011704:Pyelonephritis / Q000382:microbiology; D014398:Tuberculosis, Renal / Q000209:etiology* / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D014517:Ureteral Obstruction / Q000382:microbiology