DOI: 10.1148/rg.241035071
(Radiographics. 2004;24:251-256.)
© RSNA, 2004
Renal Tuberculosis1
Michael S. Gibson, MD,
Michael L. Puckett, MD and
Mark E. Shelly, MD
1 From the Department of Radiology, Naval Medical Center San Diego, 34800 Bob Wilson Dr, Bldg 1, 2nd Fl, San Diego, CA 92134. Received March 17, 2003; revision requested April 16 and received June 16; accepted June 16. Address correspondence to M.S.G. (e-mail: drgibby7@cox.net).
Index Terms: Kidney, diseases, 81.23 • Tuberculosis, genitourinary, 81.23
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History
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A 55-year-old woman presented with a 3-month history of recurrent episodes of dysuria and gross hematuria. The patient had a remote history of positive purified protein derivative skin test results but had never received treatment for tuberculosis. Urinalysis revealed too-numerous-to-count white and red blood cells but no growth on multiple urine cultures. The patient showed minimal symptomatic improvement after two courses of levofloxacin and one course of nitrofurantoin. Contrast material–enhanced computed tomography (CT) of the abdomen was performed for further evaluation of the persistent hematuria and pyuria. Mycobacterium tuberculosis was isolated at acid-fast bacteria urine culture. The patient was started on a multidrug therapeutic regimen, which was well tolerated initially. During the course of treatment, mild hepatotoxicity developed, as evidenced by elevated liver transaminase levels.
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Imaging Findings
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Unenhanced helical CT of the abdomen demonstrated large, globular high-attenuation areas in the upper pole of the right kidney (Fig 1). Contrast-enhanced nephrographic-phase CT showed cortical thinning with markedly dilated calices that appeared to communicate with the globular high-attenuation areas (Fig 2a). The right ureter was thickened and demonstrated abnormal mural enhancement (Fig 2b). The left kidney was unremarkable. Delayed excretory-phase CT revealed infundibular narrowing as well as long-segment mural thickening, luminal narrowing, and irregularity of the right ureter (Fig 3).
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Figure 2a. (a) Contrast-enhanced nephrographic-phase CT scan shows dilated calices and thinning of the renal cortex (arrow). (b) Magnified view from a contrast-enhanced nephrographic-phase CT scan obtained caudad to a shows mural enhancement and thickening of the proximal ureter (arrow).
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Figure 2b. (a) Contrast-enhanced nephrographic-phase CT scan shows dilated calices and thinning of the renal cortex (arrow). (b) Magnified view from a contrast-enhanced nephrographic-phase CT scan obtained caudad to a shows mural enhancement and thickening of the proximal ureter (arrow).
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Figure 3a. (a) Contrast-enhanced excretory-phase CT scan shows dilated calices and narrowing of the infundibula (arrowheads). (b) Contrast-enhanced excretory-phase CT scan obtained at the level of the midureter shows circumferential ureteral wall thickening (arrow). The left ureter is normal (arrowhead).
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Figure 3b. (a) Contrast-enhanced excretory-phase CT scan shows dilated calices and narrowing of the infundibula (arrowheads). (b) Contrast-enhanced excretory-phase CT scan obtained at the level of the midureter shows circumferential ureteral wall thickening (arrow). The left ureter is normal (arrowhead).
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Retrograde ureteropyelography showed an atrophic right kidney with diffuse caliceal dilatation, papillary necrosis, and infundibular narrowing (Fig 4a). Mucosal irregularities were present along the length of the rigid, straightened, stemlike right ureter (Fig 4b).
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Figure 4a. (a) Retrograde ureteropyelogram shows globular calcific areas of increased opacity in the medial upper pole of the right kidney (arrowheads). The calices are markedly enlarged with ill-defined margins (white arrows). Small, irregular collections of extracaliceal contrast material are also present (black arrows). (b) Magnified view from a retrograde ureteropyelogram of the right ureter shows mucosal irregularities and erosions (arrowheads).
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Figure 4b. (a) Retrograde ureteropyelogram shows globular calcific areas of increased opacity in the medial upper pole of the right kidney (arrowheads). The calices are markedly enlarged with ill-defined margins (white arrows). Small, irregular collections of extracaliceal contrast material are also present (black arrows). (b) Magnified view from a retrograde ureteropyelogram of the right ureter shows mucosal irregularities and erosions (arrowheads).
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Nuclear scintigraphy of the kidney with technetium-99m mercaptoacetyltriglycine revealed only 7% relative function in the atrophic right kidney.
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Pathologic Evaluation
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A laparoscopic right nephroureterectomy was performed with the goal of shortening the duration of required medical therapy. At macroscopic examination, the gross pathologic specimen had a multinodular yellow-gray surface. Bivalving of the kidney revealed a 2.5 x 2.5-cm area of caseous necrosis in the upper pole (Fig 5), accounting for the CT finding of globular areas of increased attenuation. The calices were dilated, a finding that corresponded to the findings at both CT and retrograde ureteropyelography.
Histologic examination showed caseating granulomatous inflammation and chronic interstitial inflammation with focal thyroidization of the cortical tubules and associated focal segmental glomerular sclerosis (Fig 6), findings that are consistent with chronic pyelonephritis. Although findings at special staining for acid-fast organisms and fungi were negative, the patient’s history of positive acid-fast bacteria urine culture coupled with the presence of caseating granulomatous inflammation led to a diagnosis of renal tuberculosis.
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Figure 6. Low-power photomicrograph (original magnification, x10; hematoxylin-eosin stain) shows focal caseating granulomas (arrows) and sheets of chronic interstitial inflammation (arrowhead).
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Discussion
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Tuberculosis remains the most common worldwide cause of mortality from infectious disease. The World Health Organization estimates that 2 million people die from tuberculosis each year, with an additional 6 million people developing active disease. Approximately one-third of the world’s population is believed to harbor latent infection with M tuberculosis. Although over 90% of cases occur in developing countries, approximately 15 million individuals in the United States are infected (1).
The genitourinary system is one of the most common sites of involvement by extrapulmonary tuberculosis, accounting for 15%–20% of infections outside the lungs (1,2). Approximately 4%–8% of patients with pulmonary tuberculosis will develop clinically significant genitourinary infection (3,4). About 25% of patients who present with tuberculous genitourinary disease have a known history of prior pulmonary tuberculosis; an additional 25%–50% of patients will have radiographic evidence of prior subclinical pulmonary infection (4).
Tuberculosis of the kidney results from hematogenous seeding of M tuberculosis in the glomerular and peritubular capillary bed from a pulmonary site of primary infection (3–5). Small granulomas form in the renal cortex bilaterally, adjacent to the glomeruli. A high rate of perfusion and favorable oxygen tension increase the likelihood of bacilli proliferating in this location (4). In patients with intact cellular immunity, there is inhibition of bacterial duplication with confinement of the disease process to the cortex (6). Multiple bilateral cortical granulomas can remain asymptomatic and dormant for decades (3–5). In some patients, breakdown of host defense mechanisms leads to reactivation of the cortical granulomas with enlargement and coalescence (4). Capillary rupture results in delivery of organisms to the proximal tubule and loop of Henle with eventual development of enlarging, caseating granulomas and papillary necrosis (4). Granuloma formation, caseous necrosis, and cavitation are stages of progressive infection, which can eventually destroy the entire kidney. Communication of the granulomas with the collecting system can lead to regional spread of the bacilli into the renal pelvis, ureters, urinary bladder, and accessory genital organs. The host’s healing response induces fibrosis, calcium deposition, and stricture formation, which may contribute significantly to obstruction and progressive renal dysfunction (4). Despite hematogenous seeding of both kidneys, clinically significant disease is usually limited to one side (5).
Patients with genitourinary tuberculosis typically have local symptoms including frequent voiding and dysuria. Hematuria can be either microscopic or macroscopic. Symptoms may also include back, flank, or abdominal pain (7–9). Constitutional symptoms such as fever, weight loss, fatigue, and anorexia are less common (7–9). There is often a long latency period (5–40 years) between initial infection and expression of genitourinary disease (9). Laboratory abnormalities include pyuria, proteinuria, and hematuria (9). Standard urine cultures can be normal. Furthermore, the presence of routine urinary tract pathogens can delay the diagnosis of coexistent tuberculosis. To evaluate for genitourinary tuberculosis, at least three first-morning-void urine samples should be collected for acid-fast staining and mycobacterial cultures. First-morning-void specimens are preferred over 24-hour urine collections because mycobacterial viability decreases with prolonged exposure to acid urine (4). M tuberculosis is isolated from the urine in 80%–95% of patients with genitourinary tuberculosis (8,9). Purified protein derivative skin test results will be positive in nearly all patients but clearly are not specific for genitourinary involvement.
Imaging findings can support the diagnosis of genitourinary tuberculosis, although cultures or histologic analysis is required for definitive diagnosis. Renal calcifications are a common manifestation of tuberculosis at conventional radiography, occurring in 24%–44% of patients (10). Extensive parenchymal calcification in a nonfunctioning, autonephrectomized kidney (putty kidney) is characteristic of end-stage tuberculosis (11). Calcifications may also be amorphous, granular, or curvilinear, typically within the renal parenchyma (11,12). Focal globular calcification involving an entire renal lobe is frequently associated with a granulomatous mass (10). Triangular ringlike calcifications within the collecting system are characteristic of papillary necrosis (13). Other extrapulmonary manifestations of mycobacterial disease, such as mesenteric lymph node and adrenal calcifications, as well as spinal abnormalities, may be visible on conventional radiographs. These additional findings can lend support to the diagnosis of renal tuberculosis (4).
Intravenous urography can show a broad range of findings, depending on the severity of infection. Approximately 10%–15% of patients who present with active renal tuberculosis will have normal urographic findings (14). Parenchymal scars are common, being seen in over 50% of patients (10). Irregularity of the papillary tips secondary to necrotizing papillitis ("moth-eaten" calices) is an early finding (10). Small cavities in the papillae can progress to become medullary cavities that communicate with the collecting system (4). Papillary cavitation results in the spread of infection to the urothelium and submucosa of the draining calix. A fibrotic reaction develops, which causes stenosis and strictures of the caliceal infundibula (4). Infundibular strictures can lead to localized caliectasis or incomplete opacification of the calix (phantom calix) (11,15). Some patients may present with generalized hydronephrosis (15). Scarring can cause sharp angulation of the renal pelvis (Kerr kink) (3). Ureteral involvement occurs due to the passage of infected urine. Such involvement first manifests as dilatation and mucosal irregularity (sawtooth ureter), which may progress, with advanced disease, to the formation of strictures and ureteral shortening (pipe-stem ureter) (11). Fusion of multiple strictures may create a long, irregular narrowing. Several nonconfluent strictures can produce a "beaded" or "corkscrew" ureter (3). Reduced bladder capacity is the most common finding in tuberculous cystitis. The bladder may be diminutive and irregular with advanced disease (thimble bladder) (12).
CT is helpful in determining the extent of renal and extrarenal spread of disease (6,16). CT is the most sensitive modality for identifying renal calcifications, which occur in over 50% of cases of genitourinary tuberculosis (3). Coalesced cortical granulomas containing either caseous or calcified material are readily identified at CT. Calices that are dilated and filled with fluid have an attenuation between 0 and 10 HU; debris and caseation, between 10 and 30 HU; putty-like calcification, between 50 and 120 HU; and calculi, greater than 120 HU (6). Cortical thinning is a common CT finding and may be either focal or global (6). Parenchymal scarring is readily apparent at CT. Fibrotic strictures of the infundibula, renal pelvis, and ureters may be seen at contrast-enhanced CT and are highly suggestive of tuberculosis. CT is not as sensitive as excretory urography in the detection of early urothelial mucosal changes but is useful in determining the extent of renal and extrarenal spread of infection (3,16).
Prior to the advent of the antituberculous drug era, extirpative surgery was the only treatment available for patients with genitourinary tuberculosis (8). Without surgery, the 5-year survival rate of patients with renal tuberculosis was 15%–42%; surgical intervention increased the 10-year survival rate to approximately 50% (17). Early continuous multidrug chemotherapeutic regimens were successful in reducing mortality to a rate of 2.2% (18). The current standard of care for drug-sensitive urinary tract tuberculosis in a compliant patient consists of a 6-month regimen of isoniazid and rifampin, with pyrazinamide added for the first 2 months (4). A fourth drug—ethambutol hydrochloride, streptomycin, or one of the fluoroquinolones—is typically included unless the possibility of drug resistance is exceedingly small (4). Despite treatment, strictures of the infundibula and ureters can progress secondary to the body’s healing response. Surgical intervention is indicated for management of complications, including ureteral strictures (4). The issue of nephrectomy for management of a nonfunctioning end-stage tuberculous kidney is controversial. Several authors maintain that a 2-year course of medical treatment can sterilize the end-stage kidney (19), whereas others believe that the sequestered, caseous material should be removed to shorten the duration of medical therapy and to prevent late tuberculous reactivation (20).
The differential diagnosis for the imaging appearance of renal tuberculosis includes chronic pyelonephritis, papillary necrosis, medullary sponge kidney, caliceal diverticulum, renal cell carcinoma, transitional cell carcinoma, and xanthogranulomatous pyelonephritis (7,12). The most valuable radiologic feature of genitourinary tuberculosis is the multiplicity of abnormal findings (3,4,6,16). Whenever a pattern of chronic renal inflammatory disease is recognized, particularly in the setting of periureteric or peripelvic fibrosis, tuberculosis must be considered clinically (6).
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- Leder RA, Low VH. Tuberculosis of the abdomen. Radiol Clin North Am 1995; 33:691-705.[Medline]
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- Medlar EM. Cases of renal infection in pulmonary tuberculosis: evidence of healed tuberculosis lesions. Am J Pathol 1926; 2:401-413.
- Goldman SM, Fishman EK, Hartman DS, Kim YC, Siegelman SS. Computed tomography of renal tuberculosis and its pathological correlates. J Comput Assist Tomogr 1985; 9:771-776.[Medline]
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- Kenney PJ. Imaging of chronic renal infections. AJR Am J Roentgenol 1990; 155:485-494.[Free Full Text]
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History
Imaging Findings
