RG f Volume 24 ● Number 1
RadioGraphics
Renal Tuberculosis1
Michael S. Gibson, MD ● Michael L. Puckett, MD ● Mark E. Shelly, MD
Figure 1. Unenhanced CT scan shows two large cal-
cifications in the medial upper pole of the right kidney
(arrows).
History
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 re-
sults but had never received treatment for tuber-
culosis. Urinalysis revealed too-numerous-to-
count white and red blood cells but no growth on
multiple urine cultures. The patient showed mini-
mal symptomatic improvement after two courses
Index terms: Kidney, diseases, 81.23 ● Tuberculosis, genitourinary, 81.23
RadioGraphics 2004; 24:251–256 ● Published online 10.1148/rg.241035071
1From 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).
©
RSNA, 2004
Gibson et al 251
of levofloxacin and one course of nitrofurantoin.
Contrast material– enhanced computed tomogra-
phy (CT) of the abdomen was performed for fur-
ther 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 devel-
oped, as evidenced by elevated liver transaminase
levels.
Imaging Findings
Unenhanced helical CT of the abdomen demon-
strated large, globular high-attenuation areas in
the upper pole of the right kidney (Fig 1). Con-
trast-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 unre-
markable. Delayed excretory-phase CT revealed
infundibular narrowing as well as long-segment
mural thickening, luminal narrowing, and irregu-
larity of the right ureter (Fig 3).
 252 January-February 2004 RG f Volume 24 ● Number 1

RadioGraphics

Figures 2, 3. (2a) Contrast-enhanced nephrographic-phase CT scan shows dilated calices and thin-
ning of the renal cortex (arrow). (2b) Magnified view from a contrast-enhanced nephrographic-phase
CT scan obtained caudad to a shows mural enhancement and thickening of the proximal ureter (arrow).
(3a) Contrast-enhanced excretory-phase CT scan shows dilated calices and narrowing of the infundibula
(arrowheads). (3b) 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).

Retrograde ureteropyelography showed an Pathologic Evaluation

atrophic right kidney with diffuse caliceal dilata-
tion, papillary necrosis, and infundibular narrow-
ing (Fig 4a). Mucosal irregularities were present
along the length of the rigid, straightened, stem-
like right ureter (Fig 4b).
Nuclear scintigraphy of the kidney with tech-
netium-99m mercaptoacetyltriglycine revealed
only 7% relative function in the atrophic right
kidney.
A laparoscopic right nephroureterectomy was
performed with the goal of shortening the dura-
tion 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 ⫻ 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.
 RG f Volume 24 ● Number 1 Gibson et al 253

RadioGraphics

Figure 4. (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 ure-
teropyelogram of the right ureter shows mucosal irregularities and erosions (arrowheads).

Figure 6. Low-power photomicrograph (original

Figure 5. Photograph of the bivalved
resected specimen shows two foci of case-
ous necrosis in the upper pole (arrows).
Histologic examination showed caseating
granulomatous inflammation and chronic inter-
stitial inflammation with focal thyroidization of
the cortical tubules and associated focal segmen-
tal glomerular sclerosis (Fig 6), findings that are
consistent with chronic pyelonephritis. Although
magnification, ⫻10; hematoxylin-eosin stain) shows
focal caseating granulomas (arrows) and sheets of
chronic interstitial inflammation (arrowhead).
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 in-
flammation led to a diagnosis of renal tuberculo-
sis.
 254 January-February 2004
RadioGraphics Discussion
Tuberculosis remains the most common world-
wide 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, approxi-
mately 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 infec-
tions 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 tubercu-
losis; an additional 25%–50% of patients will
have radiographic evidence of prior subclinical
pulmonary infection (4).
Tuberculosis of the kidney results from hema-
togenous seeding of M tuberculosis in the glomeru-
lar and peritubular capillary bed from a pulmo-
nary site of primary infection (3–5). Small granu-
lomas form in the renal cortex bilaterally, adjacent
to the glomeruli. A high rate of perfusion and fa-
vorable 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 bilat-
eral cortical granulomas can remain asymptom-
atic and dormant for decades (3–5). In some pa-
tients, 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 pro-
gressive infection, which can eventually destroy
the entire kidney. Communication of the granulo-
mas with the collecting system can lead to re-
RG f Volume 24 ● Number 1
gional spread of the bacilli into the renal pelvis,
ureters, urinary bladder, and accessory genital
organs. The host’s healing response induces fi-
brosis, calcium deposition, and stricture forma-
tion, which may contribute significantly to ob-
struction 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 typi-
cally have local symptoms including frequent
voiding and dysuria. Hematuria can be either mi-
croscopic 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 genito-
urinary disease (9). Laboratory abnormalities in-
clude pyuria, proteinuria, and hematuria (9).
Standard urine cultures can be normal. Further-
more, the presence of routine urinary tract patho-
gens can delay the diagnosis of coexistent tuber-
culosis. To evaluate for genitourinary tuberculo-
sis, at least three first-morning-void urine samples
should be collected for acid-fast staining and my-
cobacterial cultures. First-morning-void speci-
mens are preferred over 24-hour urine collections
because mycobacterial viability decreases with
prolonged exposure to acid urine (4). M tuberculo-
sis is isolated from the urine in 80%–95% of pa-
tients with genitourinary tuberculosis (8,9). Puri-
fied 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 diag-
nosis. Renal calcifications are a common manifes-
tation of tuberculosis at conventional radiogra-
phy, occurring in 24%– 44% of patients (10).
Extensive parenchymal calcification in a nonfunc-
tioning, autonephrectomized kidney (putty kid-
ney) 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 associ-
ated with a granulomatous mass (10). Triangular
ringlike calcifications within the collecting system
are characteristic of papillary necrosis (13). Other
 RG f Volume 24 ● Number 1
RadioGraphics extrapulmonary manifestations of mycobacterial
disease, such as mesenteric lymph node and ad-
renal calcifications, as well as spinal abnormali-
ties, 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 infec-
tion. 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 pa-
tients (10). Irregularity of the papillary tips sec-
ondary 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 sys-
tem (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 pa-
tients may present with generalized hydronephro-
sis (15). Scarring can cause sharp angulation of
the renal pelvis (Kerr kink) (3). Ureteral involve-
ment 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 non-
confluent strictures can produce a “beaded” or
“corkscrew” ureter (3). Reduced bladder capacity
is the most common finding in tuberculous cysti-
tis. 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 calci-
fications, 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 attenua-
tion 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
Gibson et al 255
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 de-
tection of early urothelial mucosal changes but is
useful in determining the extent of renal and ex-
trarenal 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 tubercu-
losis (8). Without surgery, the 5-year survival rate
of patients with renal tuberculosis was 15%– 42%;
surgical intervention increased the 10-year sur-
vival rate to approximately 50% (17). Early con-
tinuous 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 fluoro-
quinolones—is typically included unless the pos-
sibility 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 indi-
cated for management of complications, includ-
ing ureteral strictures (4). The issue of nephrec-
tomy 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, case-
ous material should be removed to shorten the
duration of medical therapy and to prevent late
tuberculous reactivation (20).
The differential diagnosis for the imaging ap-
pearance of renal tuberculosis includes chronic
pyelonephritis, papillary necrosis, medullary
sponge kidney, caliceal diverticulum, renal cell
carcinoma, transitional cell carcinoma, and xan-
thogranulomatous pyelonephritis (7,12). The
most valuable radiologic feature of genitourinary
tuberculosis is the multiplicity of abnormal find-
ings (3,4,6,16). Whenever a pattern of chronic
 256 January-February 2004
RadioGraphics renal inflammatory disease is recognized, particu-
larly in the setting of periureteric or peripelvic
fibrosis, tuberculosis must be considered clini-
cally (6).
References
1. World Health Organization. Stop TB annual re-
port 2001. Geneva, Switzerland: World Health
Organization, 2002.
2. Farer LS, Lowell AM, Meador MP. Extrapulmo-
nary tuberculosis in the United States. Am J Epi-
demiol 1979; 109:205–217.
3. Leder RA, Low VH. Tuberculosis of the abdo-
men. Radiol Clin North Am 1995; 33:691–705.
4. Pasternak MS, Rubin RH. Urinary tract tubercu-
losis. In: Schrier RW, ed. Diseases of the kidney
and urinary tract. 7th ed. Philadelphia, Pa: Lippin-
cott Williams & Wilkins, 2001; 1017–1037.
5. Medlar EM. Cases of renal infection in pulmonary
tuberculosis: evidence of healed tuberculosis le-
sions. Am J Pathol 1926; 2:401– 413.
6. Goldman SM, Fishman EK, Hartman DS, Kim
YC, Siegelman SS. Computed tomography of re-
nal tuberculosis and its pathological correlates.
J Comput Assist Tomogr 1985; 9:771–776.
7. Narayana A. Overview of renal tuberculosis. Urol-
ogy 1982; 19:231–237.
8. Simon HB, Weinstein AJ, Pasternak MS, Swartz
MN, Kunz LJ. Genitourinary tuberculosis: clinical
features in a general hospital population. Am J
Med 1977; 63:410 – 420.
9. Christensen WI. Genitourinary tuberculosis: re-
view of 102 cases. Medicine (Baltimore) 1974;
53:377–390.
RG f Volume 24 ● Number 1
10. Kollins SA, Hartman GW, Carr DT, Segura JW,
Hattery RR. Roentgenographic findings in urinary
tract tuberculosis: a 10 year review. Am J Roent-
genol Radium Ther Nucl Med 1974; 121:487–
499.
11. Engin G, Acunas B, Acunas G, Tunaci M. Imag-
ing of extrapulmonary tuberculosis. RadioGraph-
ics 2000; 20:471– 488.
12. Harisinghani MG, McLoud TC, Shepard JA, Ko
JP, Shroff MM, Mueller PR. Tuberculosis from
head to toe. RadioGraphics 2000; 20:449 – 470.
13. Davidson AJ, Hartman DS, Choyke PL, Wagner
BJ. Parenchymal disease with normal size and con-
tour. In: Davidson AJ, ed. Davidson’s radiology of
the kidney and genitourinary tract. 3rd ed. Phila-
delphia, Pa: Saunders, 1999; 327–358.
14. Kenney PJ. Imaging of chronic renal infections.
AJR Am J Roentgenol 1990; 155:485– 494.
15. Roylance J, Penry JB, Davies ER, Roberts M. The
radiology of tuberculosis of the urinary tract. Clin
Radiol 1970; 21:163–170.
16. Wang LJ, Wong YC, Chen CJ, Lim KE. CT fea-
tures of genitourinary tuberculosis. J Comput As-
sist Tomogr 1997; 21:254 –258.
17. Sporer H, Oppenheimer GD. Renal tuberculosis. J
Mt Sinai Hosp 1956; 23:521–536.
18. Gow JG. Results of treatment in a large series of
cases of genito-urinary tuberculosis and the chang-
ing pattern of the disease. Br J Urol 1970; 42:647–
655.
19. Bloom S, Wechsler H, Lattimer JK. Results of a
long-term study of non-functioning tuberculous
kidneys. J Urol 1970; 104:654 – 657.
20. Wong SH, Lau WY, Poon GP, et al. The treat-
ment of urinary tract tuberculosis. J Urol 1984;
131:297–301.