Tuberculosis y Enfermedad Renal

8/17/2015
Renal disease in tuberculosis
Official reprint from UpToDate

www.uptodate.com 2015 UpToDate

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: Jul 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
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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
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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".)
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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 the HIV-infected patient" 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
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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.)
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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 the HIV-infected patient".)
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17. Hillemann D, Rsch-Gerdes S, Boehme C, Richter E. Rapid molecular detection of extrapulmonary tuberculosis by the automated GeneXpert
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18. Becker JA. Renal tuberculosis. Urol Radiol 1988; 10:25.
19. Kollins SA, Hartman GW, Carr DT, et al. Roentgenographic findings in urinary tract tuberculosis. A 10 year review. Am J Roentgenol Radium Ther
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20. Huang LH, Wen MC, Hung SW, et al. Renal tuberculosis presenting as a complicated renal cyst. Urology 2012; 80:e69.
21. Teo EY, Wee TC. Images in clinical medicine: Renal tuberculosis. N Engl J Med 2011; 365:e26.
22. Javaud N, Belenfant X, Stirnemann J, et al. Renal granulomatoses: a retrospective study of 40 cases and review of the literature. Medicine
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23. Chapagain A, Dobbie H, Sheaff M, Yaqoob MM. Presentation, diagnosis, and treatment outcome of tuberculous-mediated tubulointerstitial nephritis.
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24. Latus J, Amann K, Braun N, et al. Tubulointerstitial nephritis in active tuberculosis - a single center experience. Clin Nephrol 2012; 78:297.
25. Eastwood JB, Corbishley CM, Grange JM. Tuberculosis and tubulointerstitial nephritis: an intriguing puzzle. Kidney Int 2011; 79:579.
26. Sun L, Yuan Q, Feng J, et al. Be alert to tuberculosis-mediated glomerulonephritis: a retrospective study. Eur J Clin Microbiol Infect Dis 2012;
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27. Kennedy AC, Burton JA, Allison ME. Tuberculosis as a continuing cause of renal amyloidosis. Br Med J 1974; 3:795.
28. le Roux DM, Pillay K, Nourse P, et al. Systemic amyloidosis complicating multidrug-resistant tuberculosis in childhood. Pediatr Infect Dis J 2012;
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29. Falck HM, Trnroth T, Wegelius O. Predominantly vascular amyloid deposition in the kidney in patients with minimal or no proteinuria. Clin Nephrol
1983; 19:137.
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31. Berns JS, Cohen RM, Stumacher RJ, Rudnick MR. Renal aspects of therapy for human immunodeficiency virus and associated opportunistic
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36. Gokce G, Kilicarslan H, Ayan S, et al. Genitourinary tuberculosis: a review of 174 cases. Scand J Infect Dis 2002; 34:338.
37. Gow JG. Results of treatment in a large series of cases of genito-urinary tuberculosis and the changing pattern of the disease. Br J Urol 1970;
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38. Psihramis KE, Donahoe PK. Primary genitourinary tuberculosis: rapid progression and tissue destruction during treatment. J Urol 1986; 135:1033.
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Topic 8003 Version 10.0
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GRAPHICS
Urinary tract tuberculosis
Intravenous pyelogram in urinary trac t tuberc ulosis. Both upper and

lower trac t involvement are present on the left side as manifested by
blunting of the c alyc es (c aliec tasis) and two long ureteral stric tures
(arrows). Although the c alic eal c hanges c an be seen in other
disorders (suc h as reflux nephropathy), the c onc urrent ureteral
abnormalities are virtually diagnostic of tuberc ulosis. 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
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Renal tuberculosis
A small, nonfunc tioning right kidney c ontaining c alc ific 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.
Graphic 88249 Version 1.0
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Disclosures
Disclosures: Vernon M Pais, Jr, MD Nothing to disclose. Jodie Dionne-Odom , MD Nothing to disclose. C Fordham von Reyn, MD
Nothing to disclose. Gary C Curhan, MD, ScD Consultant/Advisory Boards: AstraZeneca [Gout (Lesinurad)]; Allena Pharmaceuticals [Kidney
stones (Oral oxalate degrading product)]. Other Financial Interest: American Society of Nephrology [CJASN Editor-in-Chief]. Elinor L Baron,
MD, DTMH Nothing to disclose. Alice M Sheridan, MD Nothing to disclose.
Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a
multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy
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Renal disease in tuberculosis

Official reprint from UpToDate

Renal disease in tuberculosis

Renal disease in tuberculosis

Renal disease in tuberculosis

Renal disease in tuberculosis

Renal disease in tuberculosis

Renal disease in tuberculosis

Renal disease in tuberculosis

Nucl Med 1974; 121:487.

Renal disease in tuberculosis

Intravenous pyelogram in urinary trac t tuberc ulosis. Both upper and

Renal disease in tuberculosis

Renal disease in tuberculosis

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