Renal disease in tuberculosis
- Vernon M Pais, Jr, MD
Vernon M Pais, Jr, MD
- Assistant Professor of Surgery/Urology
- Geisel School of Medicine at Dartmouth
- Jodie Dionne-Odom, MD
Jodie Dionne-Odom, MD
- Assistant Professor of Medicine
- Division of Infectious Diseases
- University of Alabama at Birmingham
- Section Editors
- C Fordham von Reyn, MD
C Fordham von Reyn, MD
- Section Editor — Tuberculosis
- Section Editor — Nontuberculous Mycobacterial Infections
- Professor of Medicine
- Geisel School of Medicine at Dartmouth
- Gary C Curhan, MD, ScD
Gary C Curhan, MD, ScD
- Section Editor — Chronic Kidney Disease
- Professor of Medicine
- Harvard Medical School
Tuberculosis may lead to renal dysfunction via a range of mechanisms; these include direct infection of the kidney and lower urinary tract, tubulointerstitial nephritis, glomerulonephritis, secondary amyloidosis, and obstructive uropathy. Associated adverse effects include mild hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by pulmonary involvement and nephrotoxicity induced by antimycobacterial agents.
TUBERCULOUS URINARY TRACT INFECTION
Genitourinary tuberculosis (TB) is a common form of extrapulmonary disease; an estimated 4 to 20 percent of individuals with pulmonary infection develop genitourinary involvement, mostly in developing countries [1,2]. Genitourinary TB is more common in men than in women. Hematogenous seeding at the time of primary pulmonary infection can lead to renal involvement; infection can also occur in the setting of late reactivation disease or miliary disease. Of patients with miliary disease, 25 to 62 percent have been documented to have concomitant renal lesions . (See "Clinical manifestations, diagnosis, and treatment of extrapulmonary and miliary tuberculosis" and "Epidemiology and pathology of extrapulmonary and miliary tuberculosis".)
Mycobacterial seeding leads to granuloma formation in proximity to glomeruli. These may heal with fibrosis in the absence of overt renal disease. Alternatively, the granulomas may caseate and rupture into the tubular lumen; this can occur up to 30 years after the initial infection. Subsequently, tuberculous bacilli can enter the medullary interstitium, leading to granuloma formation and progressive medullary injury [4,5]. Destruction of renal papilla can lead to calyceal ulceration or abscess formation. Involvement of the collecting system may result in fibrotic scarring and stenosis.
Clinical manifestations — The onset of genitourinary TB is usually insidious, presenting with malaise and lower urinary tract symptoms, including dysuria and gross hematuria [4-6]. Renal colic is an uncommon manifestation. Systemic symptoms (fever, weight loss) are relatively rare, since rupture of the glomerular granulomas occurs independently of disease activity at other sites [4,7]. Some patients are asymptomatic; in such cases, pyuria and/or microscopic hematuria may be observed as incidental findings.
Pyuria and/or microscopic hematuria are present in more than 90 percent of cases . Heavy proteinuria and cellular casts are not generally seen, and the plasma creatinine concentration is usually normal. Ureteral stricture can occur and may cause obstructive uropathy [7,8]. TB can also cause chronic epididymitis or prostatitis and should be considered in cases that fail to respond to antibacterial therapy. Infertility can occur in the setting of tuberculous involvement of seminal vesicles and ejaculatory ducts in men and fallopian tubes in women . Late presentation of genitourinary TB with end-stage renal disease can be irreversible .
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- TUBERCULOUS URINARY TRACT INFECTION
- Clinical manifestations
- - Urine studies
- - Radiography
- ASSOCIATED CONDITIONS
- Tuberculous interstitial nephritis
- Tuberculous glomerulonephritis
- Secondary amyloidosis
- Drug-induced nephrotoxicity
- M. bovis infection due to intravesical BCG