Renal disease in tuberculosis

Authors
Vernon M Pais, Jr, MD
Jodie Dionne-Odom, MD
Section Editors
C Fordham von Reyn, MD
Gary C Curhan, MD, ScD
Deputy Editors
Elinor L Baron, MD, DTMH
Alice M Sheridan, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2015. | This topic last updated: Apr 22, 2015.
INTRODUCTION 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 [3]. (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 [4]. 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 [1]. Late presentation of
genitourinary TB with end-stage renal disease can be irreversible [9].

Refractory hypertension is a relatively infrequent complication of renal TB. In such cases, the
elevation in blood pressure is mediated by angiotensin II and may result from intimal proliferation
of vessels in or near areas of inflammation, leading to segmental ischemia and renin release [10].
Diagnosis The diagnosis of genitourinary TB should be suspected based on symptoms, urinalysis
findings, and current or prior TB infection. Risk factors for TB and evaluation for systemic TB are
discussed further separately. (See "Epidemiology of tuberculosis", section on 'Risk factors' and
"Diagnosis of pulmonary tuberculosis in HIV-uninfected patients".)
The diagnosis of genitourinary TB is established by demonstration of tubercle bacilli in the urine;
the constellation of dysuria, sterile pyuria, hematuria, and characteristic radiographic findings are
highly suggestive of the diagnosis [6]. Concurrent bacteriuria may be observed; therefore, a positive
urine culture should not exclude the possibility of urinary TB in the setting of active TB at an
alternate site. In the absence of alternative explanation for persistent sterile pyuria, three to six urine
cultures for acid-fast bacilli (AFB) should be performed (regardless of perceived risk for TB)
together with radiography. In areas with low incidence of TB, the likelihood of renal TB is very low
in the absence of positive findings on urine studies and radiography. (See 'Radiography' below.)
The purified protein derivative tuberculin (PPD) test is used to evaluate for prior exposure to TB.
As many as 88 percent of persons with genitourinary TB have been documented to have a positive
PPD [11]; one study including 100 women with laparoscopically confirmed infection noted a
sensitivity and specificity of 55 and 80 percent, respectively [12].
There are few data evaluating the utility of interferon-gamma release assays (IGRAs) for diagnosis
of genitourinary TB. In one study including 111 Chinese patients with extrapulmonary disease and 8
with genitourinary TB, the sensitivity and specificity of the T-spot IGRA test was 100 and 67
percent, respectively [13].
Urine studies Tuberculous bacilli are shed into the urine intermittently, and AFB smear is often
negative since the cutoff for a positive smear is 5000 organisms per mL [1]. Between 11 and 80
percent of single urine specimens are positive for AFB culture in patients with active disease,
depending on the demographic group and stage of infection [1,14]. Therefore, three to six first
morning midstream specimens should be obtained for AFB culture to maximize the likelihood of a
positive result.
Identification of acid-fast organisms in the urine sediment via Ziehl-Neelsen stain or fluorescent
dye techniques is not diagnostic for TB, since nonpathogenic mycobacteria may be present [6].
False-negative results may occur in the setting of concomitant antituberculous or antibacterial
therapy capable of inhibiting mycobacterial growth (particularly fluoroquinolones) [6]. The use of
polymerase chain reaction (PCR) for detection of Mycobacterium tuberculosis in urine or renal
tissue is improving diagnostic capabilities; sensitivity and specificity are 87 to 100 percent and 93
to 98 percent, respectively [1,15,16]. Some individual laboratories offer validated testing, although,
thus far, there is no commercial nucleic acid amplification test approved by the US Food and Drug
Administration (FDA) for detection of mycobacterial nucleic acid in urine.
Data on use of the GeneXpert MTB/RIF molecular system for diagnosis of extrapulmonary TB are
limited. One study of 91 urine samples from patients with suspected TB or nontuberculous
mycobacteria infections (including five culture positive samples) noted sensitivity and specificity of
100 and 98.6 percent, respectively [17].

Radiography Radiographic studies are useful. Evidence of both upper and lower urinary tract
involvement strongly suggests the presence of genitourinary TB [18,19]. Scout films or plain
radiographs may demonstrate calcifications. Intravenous pyelography (IVP) is used for evaluation
of suspected renal TB in settings where other modalities are not available. The IVP may be normal
in early disease; by the time clinical symptoms develop, moderate to marked urinary tract
abnormalities are usually present. The earliest findings include erosion of the tips of the calyces,
narrowing of collecting system infundibula, blunting of the calyces, or overt papillary necrosis with
associated parenchymal scarring and calcification [4,18,19]. These findings may be unilateral or
bilateral and resemble those seen in chronic pyelonephritis or papillary necrosis due to other causes
such as analgesic abuse. Signs of extrarenal disease include single or multiple ureteral strictures
(image 1), a contracted bladder, and, in males, calcifications in the vas deferens, seminal vesicles, or
prostate [18,19].
Computed tomography (CT) imaging may demonstrate asymmetric caliectasis, hydronephrosis,
and/or ureteral stricture. Asymmetric caliectasis reflects uneven infundibular scarring. Caliectasis
accompanied by thickened and/or enhancing walls and calcification can mimic the appearance of
complex renal cysts [20]. Periureteral and perirenal fibrosis may also be observed. CT can be of
particular use in delineating pararenal sinus tracts and also allows identification of the
"autonephrectomized" nonfunctioning end-stage kidney that may result from extensive renal TB
damage (image 2) [2,9,21].
ASSOCIATED CONDITIONS
Tuberculous interstitial nephritis There are case reports and retrospective studies suggesting that
tuberculosis (TB) can lead to chronic interstitial nephritis in rare cases [7,22-24]. The approach to
diagnosis of tuberculous interstitial nephritis is the same as described above for tuberculous urinary
tract infection: three to six urine cultures for acid-fast bacilli (AFB), together with radiography.
Tuberculous interstitial nephritis is unlikely in the setting of negative urine culture and absence of
TB elsewhere. The pathogenesis of TB-associated interstitial nephritis is not clear; it may be an
immunological epiphenomenon induced by TB in other organs [25]. (See 'Diagnosis' above.)
In one series of 25 patients of Asian descent who presented with TB and significant renal disease,
chronic granulomatous interstitial nephritis was the primary lesion in all who underwent biopsy (68
percent) [23]. Renal biopsy revealed interstitial inflammation with eosinophilia and granulomas;
caseating granulomas were identified in three patients. There was no evidence of immune complex
deposition in any of the samples, although nonspecific mesangial immunoglobulin (Ig)G deposition
was observed. None of the biopsy specimens were positive for AFB by Ziehl-Neelsen staining or
culture. Leukocyturia was the major finding on urinalysis but was not present in all cases. Evidence
of systemic TB was observed in nine patients. In eight patients, active urine sediment and rapidly
progressive renal failure were observed, but there were no extrarenal symptoms related to TB.
Tuberculous glomerulonephritis There are case reports of patients with glomerulonephritis due
to TB. The diagnosis is difficult to establish, particularly early in disease, but is an important
consideration since treatment of glomerulonephritis with steroids can worsen underlying TB.
In one retrospective study including 46 Chinese patients with tuberculous glomerulonephritis, 76
percent had a history of pulmonary or extrapulmonary TB. Most were symptomatic with edema and
fatigue and had hematuria (67 percent) and proteinuria (70 percent); pyuria was observed in 11
percent of cases. A positive urine AFB culture was observed in 20 percent of cases and renal biopsy
was polymerase chain reaction (PCR) positive for TB in 85 percent of cases [26].

Secondary amyloidosis Secondary amyloidosis may develop in the setting of chronic

inflammation, leading to high circulating levels of serum amyloid A protein, an acute-phase
reactant. It should be suspected in patients with TB who present with nephrotic range proteinuria
[27,28]. The diagnosis of secondary amyloidosis is established by demonstrating tissue amyloid
deposition on biopsy of the abdominal fat pad, rectum, or kidney.
In contrast with secondary amyloidosis, primary vascular amyloidosis causes glomerular ischemia
but not an increase in glomerular permeability. The clinical manifestations in this setting include
slowly progressive renal failure, a benign urine sediment, and little if any proteinuria [29]. (See
"Renal amyloidosis" and "Causes and diagnosis of secondary (AA) amyloidosis and relation to
rheumatic diseases".)
Hyponatremia Mild hyponatremia (plasma sodium concentration between 125 and 135 mEq/L)
can be seen in the setting of active pulmonary or miliary TB [30]. Most patients appear to have the
syndrome of inappropriate antidiuretic hormone (ADH) secretion; approximately one-third have a
reset osmostat in which the plasma sodium concentration is stable at a new lower level. The factors
responsible for the persistent ADH release in this setting are not known, but hyponatremia and
abnormal water handling resolve following effective treatment [30]. (See "Pathophysiology and
etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)".)
Drug-induced nephrotoxicity Some antituberculous drugs can affect renal function [31].
Rifampin can induce tubular and interstitial injury and, in rare cases, can cause crescentic
glomerulonephritis [31]. Renal failure can occur within hours of the first dose but can also occur
with intermittent or discontinuous long-term therapy. Affected patients typically present with acute
renal failure with interstitial nephritis on renal biopsy. Tubular function is also abnormal and can
lead to renal glucosuria, hyperuricosuria, polyuria due to nephrogenic diabetes insipidus, and
increased urinary excretion of polyclonal light chains. The latter can rarely lead to tubular
obstruction, simulating myeloma kidney [32].
Ethambutol and pyrazinamide are not nephrotoxins but can cause a selective decrease in uric acid
excretion due to diminished secretion or enhanced reabsorption [31,33]. Hyperuricemia may be
seen in 40 to 50 percent of these patients [31]. Gout can occur, but there is no risk of acute uric acid
nephropathy, since uric acid excretion is not enhanced.
M. bovis infection due to intravesical BCG Mycobacterium bovis infection can occur in the
setting of intravesical Bacillus Calmette-Guerin (BCG) immunotherapy. Issues related to use of
intravesical BCG are discussed separately, as are issues related to diagnosis and treatment of M.
bovis infection. (See "Complications of intravesical BCG immunotherapy" and "Mycobacterium
bovis".)
TREATMENT The approach to treatment of renal tuberculosis (TB) is generally the same as that
for pulmonary TB. Appropriate treatment with standard antituberculous agents for six months is
generally successful in eradicating active renal infection due to drug-susceptible TB [34], although
dose adjustment of medications is needed in the setting of renal insufficiency. The treatment
regimen varies with whether or not the patient has HIV infection or drug-resistant TB. These issues
are discussed in detail separately. (See "Treatment of pulmonary tuberculosis in HIV-uninfected
patients" and "Treatment of pulmonary tuberculosis in HIV-infected adults" and "Diagnosis,
treatment, and prevention of drug-resistant tuberculosis".)

Clinical response to antituberculous therapy is generally favorable because of high urinary

concentrations of antituberculous agents and excellent renal vascular supply. Urine sterilization
generally occurs within two weeks of initiating therapy. In one study including seven patients with
culture-confirmed urinary tract disease treated with standard therapy, no relapse was observed [35].
Relapse rates among patients who require nephrectomy appear to be relatively low; one large study
noted a relapse rate <1 percent [3]; however, one study of 174 cases in Turkey demonstrated a
relapse rate of 19 percent even after 12 months of therapy [36].
Among 135 patients treated for renal TB in the 1960s with six months of isoniazid, streptomycin,
and paraaminosalicylic acid, 97 percent had negative follow-up urine culture after 10 years of
follow-up; 60 to 90 percent of patients required a combination of surgical and medical therapy [37].
In a follow-up study of 135 patients with renal TB who were treated with isoniazid, rifampin, and
ethambutol for six to nine months (1970 to 1974) or isoniazid, rifampin, and pyrazinamide for six
months (1975 to 1977), the cure rate was 100 percent (measured by urine sterilization); relapse
occurred in one patient.
Patients on antituberculous therapy should be monitored for signs and symptoms of upper urinary
tract obstruction (ie, flank pain, renal colic, hydronephrosis) during treatment [38]. Clinical
worsening may be observed in the first few weeks of antituberculous therapy due to inflammation,
followed by fibrosis and obstruction of the collecting system [3]. Ureteral strictures may progress
during treatment due to scarring and subsequent narrowing of the lumen [18]. In one retrospective
study including 21 kidneys in which ureteral strictures developed during the course of
antituberculous therapy, 76 percent developed within the initial two months of treatment [39]. Early
endourologic decompression with ureteral stent or percutaneous nephrostomy placement was
associated with lower nephrectomy rate compared with treatment with medication alone (27 versus
66 percent) [39].
Apart from endourologic decompression, other surgical intervention for genitourinary TB should be
delayed until the patient has received at least four weeks of antituberculosis medical therapy [40].
Delayed definitive reconstruction for stricture may include ureteral reimplantation,
ureteroureterostomy, pyeloplasty, or ureteral substitution and should be based upon the location and
length of remaining stricture. In the setting of nonfunctioning kidney and associated sequelae
including urosepsis or poorly controlled hypertension, nephrectomy should be considered [40].
SUMMARY
Among patients with pulmonary tuberculosis (TB), genitourinary involvement occurs in 4 to 20
percent of patients. Hematogenous seeding of the kidney at the time of primary TB infection leads
to granuloma formation in proximity to glomeruli, which can caseate and rupture into the tubular
lumen. Subsequently, tuberculous bacilli can enter the medullary interstitium, leading to progressive
medullary injury. Destruction of renal papilla can lead to calyceal ulceration or abscess formation.
Involvement of the collecting system may result in fibrotic scarring and stenosis. (See 'Tuberculous
urinary tract infection' above.)
The onset of genitourinary TB is usually insidious, presenting with malaise and lower urinary tract
symptoms, including dysuria and gross hematuria. Systemic symptoms (fever, weight loss) are
relatively rare, since rupture of the glomerular granulomas occurs independently of disease activity
at other sites. (See 'Clinical manifestations' above.)
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. (See 'Clinical
manifestations' above.)
The diagnosis of genitourinary TB is established by demonstration of tubercle bacilli in the urine;
the constellation of dysuria, sterile pyuria, hematuria, and characteristic radiographic findings are
highly suggestive of the diagnosis. Three to six first morning midstream specimens should be
obtained for acid-fast bacilli (AFB) culture to maximize the likelihood of a positive result. Among
patients with active renal TB, 30 to 40 percent of single urine specimens will be positive by AFB
culture. Polymerase chain reaction is also a useful diagnostic tool with 87 to 100 percent sensitivity
and 93 to 98 percent specificity. (See 'Diagnosis' above.)
Radiographic studies are useful; evidence of both upper and lower urinary tract involvement in the
form of calcifications, calyceal distortion, and infundibular and ureteral strictures strongly suggests
the presence of genitourinary TB. The earliest findings on intravenous pyelogram include erosion of
the tips of the calyces, narrowing of collecting system infundibula, blunting of the calyces, or overt
papillary necrosis with associated parenchymal scarring and calcification. (See 'Diagnosis' above.)
Associated conditions include tubulointerstitial nephritis, glomerulonephritis, secondary
amyloidosis, and obstructive uropathy. Associated adverse effects include mild hyponatremia due to
the syndrome of inappropriate antidiuretic hormone secretion induced by pulmonary involvement
and nephrotoxicity induced by antimycobacterial agents. (See 'Associated conditions' above.)
The approach to antituberculous therapy for renal TB is generally the same as that for pulmonary
TB; this is discussed in detail separately. Early endourologic decompression of affected kidney
obstructed by stricture appears to improve renal salvage rate. (See 'Treatment' above and "Treatment
of pulmonary tuberculosis in HIV-uninfected patients" and "Treatment of pulmonary tuberculosis in
HIV-infected adults".)
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Topic 8003 Version 10.0

GRAPHICS
Urinary tract tuberculosis

Intravenous pyelogram in urinary tract tuberculosis. Both upper and lower tract involvement are
present on the left side as manifested by blunting of the calyces (caliectasis) and two long ureteral
strictures (arrows). Although the caliceal changes can be seen in other disorders (such as reflux
nephropathy), the concurrent ureteral abnormalities are virtually diagnostic of tuberculosis. A
normal pelvic right kidney is also present but is not well visualized.
From Rose BD, Pathophysiology of Renal Disease, 1st ed, McGraw-Hill, New York 1981.
Graphic 64772 Version 3.0
Renal tuberculosis

A small, nonfunctioning right kidney containing calcific debris is present.

Reproduced with permission from: Daffner RH. Clinical Radiology: The Essentials, 3rd Edition.
Philadelphia: Lippincott Williams & Wilkins, 2007. Copyright 2007 Lippincott Williams &
Wilkins.