H. Öztürk et al. / Case Reports in Clinical Medicine 2 (2013) 411-414
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verity of the immunosuppression [7].
M. tuberculosis, so-called tuberculosis bacillus, is an
aerobic, non-sporing, slightly curved or smooth bacillus
0.2 − 0.6 × 1 − 10 µm in dimension [8]. The cell wall of
the tuberculosis bacillus is much thicker than other bac-
teria and contains higher amounts of lipids. The main
reason for the slow growth rate and drug resistance to
many known antibiotics which are distinctive features of
the tuberculosis bacillus is low permeability of its cell
wall. Rich lipid content as well as less passing canals on
the cell wall compared to other bacteria play an impor-
tant role in low permeability [9]. Diagnosis of the disease
is made by microbiological (direct observation, culture),
molecular (PCR, strand displacement amplification [SDA],
transcription mediated amplification [TMA], ligase chain
reaction [LCR]) and immunological (38 kDa antigen, 16
kDa antigen, QuantiFERON-TB Gold in tube and T
SPOT-TB) assays [10].
Urinary tuberculosis is a common form of extra-pul-
monary tuberculosis. It occurs especially in advanced
ages. The disease most commonly starts from the kid-
neys. The tuberculosis bacillus settles down in the renal
cortex during primary bacillemia and forms multiple
granulomatous foci. Infection is restricted at this point if
immunity is sufficient. Then, some of these lesions are
activated and medulla and papilla of the kidney are in-
volved with the advanced infectious process. Desctruc-
tive changes occur such as papillary necrosis and cavita-
tion. Typical ulcero-cavernous lesions occur subsequent-
ly to ulcerated calyces. At this point, many bacilli and
inflammatory debris are discharged into the renal pelvis
and then into the ureters and bladder [11-13]. There is no
typical clinical sign in urinary tract tuberculosis. The
patient may be asymptomatic since the infection devel-
ops slowly. Local signs are more common than systemic
ones. There is usually a complaint of frequent, painless
micturition. Renal tuberculosis rarely causes loss of renal
function but previous renal conditions may lead to the
development of renal failure. Nephrolithiasis and recur-
rent bacterial infections may develop in the kidneys
[11,14]. Diagnosis of genitourinary tuberculosis is made
by showing the bacillus in the urine or involved tissue.
There are abnormal urinary findings in 90% of patients
with renal or genital tuberculosis. The most common
findings are pyuria, hematuria, or combination of them.
Tuberculosis should be investigated if pyuria is found in
an acidic urine and no microorganism grows in routine
urinary culture. In the studies so far, radiological signs
related to previous or active tuberculosis on chest radio-
grams of 50% to 70% of patients with genitourinary tu-
berculosis [12,14]. Culture is positive in 80% - 95% of
cases of genitourinary tuberculosis. In the study by Bentz
et al. [15], association of genitourinary tuberculosis with
other forms of extra-pulmonary tuberculosis was found
in 21% of the cases. Genitourinary tuberculosis (GUTB)
was demonstrated in 5% of cases with pulmonary tuber-
culosis.
While nephrectomy was the mainstay for the man-
agement of the renal tuberculosis in the past, it is rarely
required currently. Medical treatment is successful in
renal tuberculosis and standard anti-tuberculosis treat-
ment has been recommended for 6 months. Monthly uri-
nary culture is also recommended during the treatment
until the negative culture is obtained. Nephrectomy is
among the therapeutic options in the case of recurrent
bacterial infections in the dysfunctional kidney, persist-
ing pain, massive hematuria, hypertension or infection
due to multi-drug resistant microorganisms. Surgical or
endoscopic interventions may be required to open stric-
tures in the ureters or to increase capacity of the bladder.
Nephrostomy or drainage through a stent may be per-
formed in progressive failure develops due to hydrone-
phrosis and obstruction. Use of corticosteroids in addi-
tion to a stent in ureterial stenosis is controversial [16].
Genital organ tuberculosis responds well to the anti-tu-
berculosis treatment. Surgical treatment should be con-
sidered only in the presence of pelvic masses not re-
sponding to anti-tuberculosis treatment, persisting pelvic
pain, and renal tuberculosis advanced to auto-nephrec-
tomy despite medical treatment [11,12].
2. CASE REPORT
A 66-year-old man presented to our out-patient clinic
with right flank pain and hematuria. The investigations
revealed 4 calculi 10 mm in diameter in the lower pole of
right kidney, parenchymal thinning in the lower pole.
Both kidneys were functional and both ureters were
normal in appearance. His history revealed open surgery
for renal calculi from his left kidney, total thyroidectomy,
duodenal ulcer perforation, and repair of incisional her-
nia. His laboratory findings were as follows: Glucose:
102 mg/dL; creatinine: 1.2 mg/dL; hemogram (WBC:
5400/µL; NEU: 57%; LYM: 30%; MON: 10%; Hemo-
globin: 12.3 g/dL; Hematocrit: 35%, PLT: 320,000/µL);
hepatic function tests: normal; sedimentation rate: 66/
hour; TSH: 1.1 uIU/ml; urine analysis: 30 leukocytes, 7 -
8 erythrocytes per field; Anti-HIV: negative. No bacteria
grown in urinary culture. His own and family history
didn’t reveal tuberculosis.
Pulmonary radiograms were normal. On intravenous
pyelography both kidneys were concurrently functional,
discontinuity between the right ureter and pelvis, caly-
ceal dilatation in the lower pole of right kidney and 4
renal calculi 10 mm in diameter were observed. The pa-
tient underwent PCNL upon observing multiple renal
calculi larger than 10 mm in lower pole of the right kid-
ney. Biopsy was performed during PNCL because mor-