1. GENITO-URINARY TUBERCULOSIS
DR. SWAPNIL S.TOPALE
YASHODA SUPER SPECIALITY HOSPITAL,
MALAKPET,
HYDERABAD

2. INTRODUCTION
 The term genitourinary tuberculosis was
introduced by Wildbolz in 1937, and since then,
renal and epididymal tuberculosis were
considered together as the local manifestation
of the same blood-borne infection
 In India the estimate of TB is 168/100,000
population/year (WHO 2005 estimates) with an
annual incidence of 2.2 million/year (worldwide
six million new cases) and an annual death rate
of 29/100,000 population/year

3.  In comparison to only pulmonary TB, which
comprises around 68.4%, the incidence of
combined pulmonary extrapulmonary cases and
extrapulmonary TB alone comprise 12% and 20-
25% of the total disease burden respectively
 Amongst extrapulmonary TB, GUTB accounts for
4% of the load
 In comparison to the patient’s complaints, the
sequel of genitourinary TB is volcanic and
requires proper understanding

4. INCIDENCE
Genital tract tuberculosis
 The most common form of extrapulmonary TB
is genitourinary disease
 Worldwide- 27% (range, 14 to 41%)
 India-18%
Female genital tract tuberculosis:
 1% of infertile women, aged between 20-40
years in United States and 18% in India suffer
from genital TB

5. In females the genital organs commonly affected are as
follows:
 fallopian tube (95-100%)
 endometrium (50-60%)
 ovaries (20-30%)
 cervix (5-15%)
 myometrium (2.5%)
 vulva/vagina (1%)
Male genital tuberculosis:
 associated with tuberculosis of the kidney and prostate,
seminal vesicle, epididymis, testes as well as scrotum
may occasionally be affected

6. Tuberculosis in HIV-infected patients:
 India-5.2% new cases have HIV (15-49 years) and in an
average
 Worldwide-10% of all cases of TB are HIV-related (1999
data)
Tuberculosis in post-transplant patients:
9.5-14.7% in India
Tuberculosis in children with nephrotic syndrome:
 in a study by Gulati et al., 9.3%, amongst a total of 300
children with nephrotic syndrome had renal tuberculosis

7. ETIOPATHOGENESIS
 Tuberculosis is a chronic infection, caused by different species of
Mycobacterium tuberculosis complex, such as :
• M. tuberculosis
• M. Canettii
• M. Africanum
• M. bovis,
• M. microti
• M. pinnipedii,
• M. caprae.
 Commonly, Mycobacterium tuberculosis, bovis, and africanum are
Infectious While M. tuberculosis is the major cause of TB in humans
 M. africanum sometimes causes pulmonary TB in humans in Africa.

8.  Tubercle bacilli can remain dormant in tissues
and persist for many years. Along with the type
of mycobacterial species, duration of
exposure, size and infectivity of the strain are
also responsible for the difference in infectivity
Tuberculosis in vitamin D deficiency
 There is sizeable evidence that a fall in serum
25-Ohvitamin D3 level compromises cell-
mediated immune defenses, leading to the
activation of latent tuberculosis

9. SOURCES OF GENITOURINARY TUBERCULOSIS
 At the time of primary TB, the disseminated microorganisms through
the blood stream to different organ systems remain dormant in latent
foci
 In 5-15% of infected patients, these dormant foci break down
(liquefaction necrosis and cavitation) causing dispersion of tubercle
bacilli
 This secondary disease, or reactivation TB, occurs as a consequence
of a decreased cellular immunity
 Genitourinary TB is usually caused by reactivation of these dormant
organisms, usually within the first two years following the primary
infection by M. tuberculosis (90-95%) and very rarely (5-10%) by M.
bovis, where the source of infection is the gastrointestinal tract

10. TB OF FEMALE GENITAL TRACT
 The bacilli reach the genital tract by three principal routes:
1. The hematogenous route (90%)
2. descending direct spread or
3. lymphatic spread
 rarely may occur from direct inoculation during sexual
intercourse with patients with genitourinary tuberculosis
 Trans-serosal exudation may give rise to pelvic inflammatory
disease and subsequently in extensive pelvic diseases
 Very rarely sexual transport has been reported, as 3.9% men
with GUTB harbor bacilli in semen

11. TB OF MALE GENITAL TRACT: IN MEN
 The sites most commonly involved are epididymis, followed
by the prostate,testicular involvement is less common and
usually is the result of direct extension from the epididymis
 Tubercular prostatitis usually results from antegrade infection
within the urinary tract
 Many theories have been postulated to define the precise
route of infection to the epididymis. These include -
i) Infected urine theory
ii) spread via lymphatic system and
iii) metastatic spread through the blood stream.
iv)Female to male transmission (venereal transmission of TB) is
very rare.

12.  Testicular involvement is usually as a result of
local invasion from the epididymis, retrograde
seeding from the epididymis and rarely by
hematogenous spread
 Involvement of scrotal wall suggests local
extratesticular extension of disease process
 Male genital tuberculosis usually is associated
with renal TB in 60 to 65% cases or with
pulmonary TB in around 34% cases.

13. TB OF URINARY TRACT
 In the kidney, hematogenous spread primarily involves the renal
cortex and remains dormant
 Abnormal host defense mechanism leads to reactivation of these foci
with enlargement
 Later, the abscess may rupture into the proximal tubule and loop of
Henle with eventual development of enlarging, caseating granulomas
with papillary necrosis
 Spread to the renal pelvis produces pyonephrosis-like lesion, also
known as a .cement. or .putty. kidney, which frequently spreads down
to the ureters, bladder, or urethra, resulting into ureteric strictures and
segmental dilation and Obstruction
 Tuberculosis of the ureter usually starts in the ureterovesical junction.

14. IMMUNE RESPONSE IN TUBERCULOSIS
 Though M. tuberculosis stimulates both the humoral and
cellular immune systems, the antibodies are not protective
 Activation of cellular immunity blocks and the extent of
disease within four to six weeks of initial infection and elicits
typical granulomas (also called tubercles), where
macrophages are transformed to giant epithelioid cells
 Excessive delayedtype hypersensitivity. with cytolytic T-cell
activity, leads to the degeneration of the center of the lesion
 In general, CD4+ cells (Helper T cells) form large
aggregations dominating the granulomas while the CD8+
cells (Cytotoxic T cells) are sparse and distributed more
toward the periphery of the lesion (immunosurveillance

15. PATHOLOGY OF GENITOURINARY TUBERCULOSIS
Gross pathology:
Renal TB:
 Kidneys may be involved in two ways:
1. miliary TB-multiple cortical white nodules of
around 1 mm due to hematogenous spread of
bacilli, or
2. cavitary renal TB (localized ascending
infection) and predominant medullary lesions

16.  The cortical granulomas may remain dormant, asymptomatic, and
stable for as long as 10 to 15 years
 When they coalesce, cavities are formed, which communicate with
the pelvicalyceal system via erosion (moth-eaten appearance on
ultrasonography), may rupture or cause part of the papillae to
become necrotic, which eventually sloughs out. The end result is a
destroyed, defunct calciÞ ed kidney (autonephrectomy)
 At this stage, multiple surface scars are noted on the kidney along
with dilated and deformed renal excretory system, Þ lled with
caseous necrotic material (pyonephrosis)
 Later on the only remains may be necrotic material surrounded by Þ
brous tissue, commonly called cement or putty or chalk kidney

17.  Sometimes both kidneys may be slightly enlarged
due to amyloidosis or diffuse proliferative
glomerulonephritis secondary to TB
 On the other hand, in tubercular interstitial
nephritis, the kidney is generally of normal size
and shows smooth contour
 Even urine culture is sterile. This entity can only
be diagnosed by demonstrating th granulomatous
involvement in renal interstitium.

18. Ureteral TB:
 Ureteral dilatation and a ragged irregular
appearance of the urothelium are the first signs of
ureteral TB (beaded or corkscrew ureter)
 There may be obstruction at the ureterovesical
junction or associated tuberculous cystitis and
ureteritis
 Ureteral shortening and fibrous contraction may
give rise to a golf hole orifice in the bladder

19. Urinary bladder TB:
 Urinary bladder TB may be induced either by local
instillation of BCG, which causes a sel flimiting
selflimiting, low-grade, superficial cystitis
 Bladder TB affects the mucosa near the ureteral orifice
to start with
 In advanced infection, the bladder becomes small,
irregular, contracted and calcified and eventually may
lead to nonfunctional urinary bladder (autocystectomy)
 Rarely fistulas may develop

20. FEMALE GENITAL TUBERCULOSIS
Fallopian tube
 In early phases, tube diameter is normal and
changes are noted mainly in advanced disease, in
the form of nodular transformation, mimicking
salpingitis isthmica nodosa
 Adhesion may occur between ovaries and other
pelvic organs with loss of fimbrial structures
 Patent ostia along with grossly diseased fallopian
tube are often an indicator of tubercular salpingitis

21. Endometrium:
 Diagnosis is often missed in biopsies, as the involvement can be
focal
 In widespread endometrial TB ulceration, caseous necrosis and
hemorrhage can be seen
Ovary:
 Affected in 10% cases
 Adhesion with the fimbria or formation of unilateral or bilateral
adnexal mass can be seen
 Gross caseous necrosis in ovaries is uncommon
Cervicitis:
 Grossly, the cervix can be normal, ulcerated or may present with a
mass mimicking malignancy
 External genitalia: Rarely can involve the vulva in the form of non-
healing ulcers

22. MALE GENITAL TUBERCULOSIS
Tubercular epididymitis:
 The globus minor is affected alone in around 40%
cases, owing to greater blood supply
 Bilateral involvement can be noted in 34% cases
 Grossly, the vas or epididymis may be beaded
 Rarely, discharging sinuses may develop
Prostate, testes, penis, urethra:
 Prostate may enlarge and show signs of
inflammation
 Gross caseous necrosis is often identifiable
 Testicular TB can show testicular swelling or

23. MICROSCOPIC FINDINGS
Urinary tract:
 In miliary renal TB, multiple small epitheloid granulomas
with neutrophils and necrosis are seen, along with
lymphocytes, mononuclear cells and plasma cell
infiltration
 In the chronic stage, extensive Þ brosis and widespread
calcifications are the findings
 Keratinizing squamous metaplasia may develop as a
late complication in renal pelvis and may persist even
after treatment of the active tuberculous lesion
 This may be a potential risk factor for the development

24. GROSS PHOTOGRAPH OF KIDNEY SHOWS MULTIPLE NECROTIC AREAS INVOLVING THE MEDULLA AND AT PLACES
DESTROYING RENAL CALYCES [FIGURE 1A]. CHRONIC TB PYELONEPHRITIS WITH DESTROYED RENAL CALYCES
[FIGURE 1B]. EPITHELIOID CELL GRANULOMAS WITH DENSE CHRONIC INFL AMMATORY INFI LTRATE IN RENAL
CORTEX. [FIGURES 1C, D, H AND E, X100]. FOCALMFORMATION OF LYMPHOID FOLLICLES [FIGURE 1E, H AND E, X40].
CROSS-SECTION OF URETER SHOWING ULCERATED UROTHELIUM BY A GRANULOMATOUS PROCESS [FIGURE 1F, H
AND E, X40]

25. Female genital tract:
 Similar epithelioid granulomas with Langhans giant cells
with or without necrosis are noted in functional
endometrial layer with ulceration of endometrial lining at
some places
 Gradual destruction and loss of endometrial glands are
commonly seen
 Metaplasia of endometrial lining or glands is not
uncommon
 In the absence of granulomatous inflammation,
infiltration of endometrium with plasma cells and

26.  In immunecompromised patients, granulomas may be less
well formed, organisms are readily demonstrated, and
caseous necrosis is seen less frequent
Male genital tuberculosis:
 The epitheloid granulomas in the prostate are usually
multiple and seen in the peripheral zones
 Calcification is not uncommon
 The scrotum shows variable degrees of fibrosis, epithelioid
granulomata, inflammation, sinus tracts and focal micro-
abscesses secondary to bacterial infections
 The gradual development of scrotal tubercular abscess may
give way and form ‘watermelon scrotum’

27.  In testes commonly epididymis is affected and
shows features of granulomatous inflammation
 Bilateral epididymal involvement and
concomitant testicular lesion strongly suggest
TB, especially in patients with evidence of TB
elsewhere in the body and failure to respondm
to conventional antibiotic therapy

28. Urinary bladder biopsy in TB:
 Usually contraindicated, unless the tubercles
or the ulcers are situated away from ureteral
orifice

29. CLINICAL PRESENTATION AND DIAGNOSTIC
APPROACH IN CASES
OF GENITOURINARY TUBERCULOSIS
 Kidney is usually the primary organ infected in
urinary disease, and other parts of the urinary
tract become involved by direct extension
 Epididymis in men and fallopian tubes in
women are the primary sites of genital infection
 The usual frequency of organ involvement is:
kidney, bladder, fallopian tube, and scrotum

30.  The GUTB has varied presentation and some of
the common ways are:
1. Recurrent or resistant urinary tract infection,
sterile pyuria with or without hematuria
2. Irritative voiding symptoms, i.e., frequency,
urgency, and dysuria
3. An incidental diagnosis in a known case of
tuberculosis.

31. 4. Renal (hydronephrosis/pyonephrosis) or epididymal
Mass
5. Infertility and pelvic inß ammatory disease
6. Renal failure (Chronic kidney disease due to
parenchymal infection and obstructive uropathy
7. The various other ways of presentation described are:
 flank pain with acute pyelonephritis
 non-healing sinuses, or fistulae (nephrocutaneous fistula
or vesicovaginal fistula)

32.  The most common symptoms with which the
patients have presented are in the form of
irritative voiding, which are found in more
than 50% of the patients
 The other symptoms in GUTB can be fever,
weight loss, anorexia, backache, and
abdominal pain

33. KIDNEY AND URETER
 asymptomatic, but may have chronic sterile pyuria
 Gross hematuria-10%
 microscopic hematuria-up to 50%
 Acute renal pain is rare. It usually occurs secondary to luminal
obstruction by blood clots, sloughed renal papilla, or flakes of
calcification
 Chronic dull ache may be due to infundibular, pelviureteric, or
ureteric stricture
 chronic renal failure which can be either due to renal parenchymal
destruction secondary to infection or due to obstructive uropathy

34. URINARY BLADDER
 Involvement of the bladder is usually secondary to renal infection and
is found in nearly one-third of the patients
 In the early stage, i.e., acute phase, bladder changes are usually
non-specific which gives rise to irritative voiding symptoms
 Chronic inflammation causes reduced compliance and capacity
manifesting as frequency of micturition
 Urgency develops if the bladder is extensively involved
 Those who develop thimble bladder. (due to mural Þ brosis and
contracture) may present with urinary incontinence
 Chronic inflammation and extensive fibrosis at vesicoureteric junction
result in Golfhole ureter

35. PROSTATE, PENIS, AND URETHRA
 Tuberculous prostatitis and urethritis can cause ..beefy
redness.. And superficial ulcerations on endoscopic
examination
 Dilatation of the prostatic urethra, and ..golf hole.. dilatation
of the prostatic ducts have also been reported
 Tuberculosis of the prostate may cause nodularity on digital
rectal examination (DRE) mimicking malignancy
 Sometimes, the diagnosis is made after histopathological
examination (HPE) of transurethral prostatectomy (TURP)
chips
 Very rarely, fulminating prostatic involvement can cause

36. Primary involvement of the penis:
 an ulcer clinically indistinguishable from
sexually transmitted diseases (STDs) or
malignancy
 Cavernositis and cold abscess formation
presenting as penile deformity or impotence
Urethral involvement:
 Stricture formation
 Hematospermia

37. EPIDIDYMIS AND TESTES
 Here, infection usually starts from the globus minor, as it has
a richer vascularity
 Usually presents as painful scrotal mass, which initially
cannot be distinguished clinically from epididymo-orchitis
 Orchitis sometimes can be difficult to differentiate from other
mass lesions of the testes
 Infertility due to epididymal and/or vasal obstruction
 Nodular beading of the vas is a characteristic physical
finding

38. PELVIC DISEASE IN FEMALES
 The association of tuberculosis and pelvic
disease most frequently presents as
infertility, chronic pelvic pain, alterations in
the menstrual pattern, or amenorrhea
 Adrenal glands- Adrenocortical insufÞ
ciency

39. DIAGNOSIS TESTS-URINE EXAMINATION
 Sterile pyuria is the classic finding
 Preferably, five consecutive early-morning specimens of
urine should be examined
 The yield of urine examination by smear and culture for
detecting the tubercle bacillus is low, probably because of the
intermittent shedding of the bacilli and is also observer-
dependent
 Direct smears-positive only in 30%
 Urine cultures require 6 to 8 weeks in special culture media
(Lowenstein-Jensen). Sensitivity- 80 -97%

40. RAPID IDENTIFICATION OF MYCOBACTERIUM
Radiometric systems
 Radiometric liquid culture systems (i.e.,
BACTEC®) [Becton Dickinson, USA]) give
rapid results and are highly sensitive in the
identification of mycobacterium
 But these methods have some inherent
diffculties in working with radioactive materials,
and the necessary apparatus used are really
expensive

41.  Polymerase chain reaction (PCR)
 Lets the sequence of DNA fragment from just a
few mycobacteria to be amplified in vitro such
that the amount of amplified DNA can be
visualized and identified
 Rapid, with results available within few hours
of DNA extraction from the sample
 Specificity-up to 88% and sensitivity-94%

42. IMAGING
 In spite of the fact that the definitive diagnosis
of genitourinary tuberculosis is established by
positive results on urine culture or histologic
examination, the imaging modalities make an
important part of the investigation module
X-chest and spine:
 to detect any pulmonary (active or old healed
granuloma) or spinal involvement

43. Plain X-ray abdomen:
 may show renal calcification
 Calcification rarely occurs in ureter (intraluminal),
bladder wall, or seminal vesicles
Intravenous urography:
 one of the most useful tests
 provides both anatomical as well as functional details of
the kidneys and ureters
 The earliest radiographic changes-changes in the minor
renal calyces with loss of sharpness and blunting

44.  Progression of the disease will cause – moth eaten appearance of
the calyces and lost calyx due to infundibular stenosis
 Ureters- initially dilated or become irregular in appearance followed
by stricture formation with predilection for the infundibulum,
ureteropelvic junction, and distal ureter, which are the sites for
narrowing
 At these states, the ureter looks like beaded or pipestem or even
corkscrew conÞ guration
 10 to 56% of the patients develop ureteric strictures
 Involvement of ureteric orifices in the late stages, as these become Þ
brotic and fixed, leads to the development of vesicoureteric reß ux
(VUR).

45. Computed tomography (CT scan)
 Currently, at many centers, CT is replacing IVU as
an imaging modality of choice in GUTB
 It is equally good at identifying calyceal and
infundibular abnormalities, renal parenchymal
destruction, and hydronephrosis or hydroureter
 In addition, it identifies adjacent adrenal,
retroperitoneal, prostatic, and seminal vesicle
abnormalities

46. Cystoscopy and biopsy:
 Cystoscopy is rarely indicated for diagnostic purpose
 Biopsy is needed if there is suspicion of malignancy
 It should be done only after 4-6 weeks of medical therapy to
prevent dissemination of the disease (i.e., tubercular
meningitis)
 The cystoscopic findings-reduced bladder capacity and
patulous ureteral orifice
 The positive bladder biopsy diagnostic of GUTB can be
found in up to 46% of the patients

47. Retrograde and antegrade pyelography
 There are two indications for it:
1. Ureteral catheterization to obtain urine sample for culture
for localization of the disease
2. To delineate the stricture of the lower ureter
 Percutaneous antegrade access is required if retrograde
access is unachievable or insufficient for drainage of the
kidney
 It also provides a route for obtaining urine samples from the
renal pelvis or tuberculous cavities for culture and to assess
therapeutic drug concentration at the target sites

48. Magnetic resonance imaging (MRI):
Useful in patients with-
 compromised renal function,
 pregnancy, or
 allergy to contrast media
 It gives good morphological details for the
kidneys as well as excellent delineation of the
ureters

50.  Diagnosis of GUTB on the basis of the
presence of one major and/or two minor
criteria:
 The major criteria-
1. granulomatous lesion on histopathology
2. AFB positivity in urine or histopathology
3. a positive PCR

51.  Minor criteria:
1. Changes suggestive of tuberculosis on
IVU/CT or MRI
2. hemaruria,
3. raised ESR, and/or
4. pulmonary changes of old healed
granulomas

52. SEQUEL OF GENITOURINARY TUBERCULOSIS
 Tuberculosis has a significant deteriorating effect on kidney function
 Though often unilateral to start with, cavitary renal TB can cause renal
failure in 12% patients and hypertension in 4-12% patients
 In one study it was reported that without surgery, the five-year survival rate
of patients with renal TB was 15-42% while surgical intervention increased
the 10-year survival rate to 50%
 If proved by selective renal artery renin estimation, nephrectomy reduces the
blood pressure substantially in patients complicated with hypertension
 Early continuous multidrug chemotherapeutic regimens are successful in
reducing mortality rate to 2.2%
 Of patients who die of pulmonary TB, 60% show coexistent renal TB in
autopsy

53.  Tuberculous epididymo-orchitis has a considerable
effect on fertility
 The sperm count and motility may be reduced due to
blockage of the vas and/or secondary atrophy
 The development of renal amyloidosis in TB is common
 This may not only cause renal dysfunction, but if not
taken care of, may lead to multiple organ failures
 Development of renal dysfunction in a known case of TB
is therefore a strong indication for a kidney biopsy

54. MEDICAL MANAGEMENT OF GENITOURINARY
TUBERCULOSIS
 In this era of evidence-based medicine, it is worthwhile to
mention that the first-ever randomized controlled trial (RCT)
in the history of modern medicine was conducted in the field
of TB
 Short-course combination chemotherapy (SCC) is the
standard of care for the treatment of TB
 When patients are treated with a single drug only, under the
selection pressure, these drug-resistant bacilli would emerge
eventually resulting in treatment-failure
 But, concomitant administration of a second drug would
prevent the emergence of these drugresistant bacilli and
thereby averts treatment failure

55.  The two most important facets of efficacy of
any combination regimen for the treatment of
TB are
i) rapid and complete killing of the bacillary
population resulting in cure, and
ii) prevention of relapse following successful
cure

56.  The WHO went on to declare TB a global emergency in the
year 1993 and adopted DOTS strategy to deal with the same
 In India, DOTS implementation began in the year 1993 on a
pilot basis, and large-scale expansion of DOTS began in
1997 under the aegis of the Revised National TB Control
Programm (RNTCP)
 By March 2006, 100% coverage of the nation had been
achieved
 Till date, more than 6.7 million patients with TB have been
started on DOTS, the treatment success rate has remained
consistently above the global benchmark of 85%, and about
1.2 million lives have been saved

60. DOSE MODIFICATION IN RENAL FAILURE
 Doses of INH, rifampicin, and pyrazinamide need no
adjustment in a patient with renal failure since these
drugs are either eliminated almost entirely through biliary
secretion or metabolized to nontoxic compounds
 The dosing interval for ethambutol has to be doubled in
patients with advanced renal failure (creatinine
clearance <10 mL/min)
 Patients with renal failure may develop peripheral
neuropathy with INH more commonly and hence should
receive pyridoxine supplementation (10 mg/day) as a
preventive measure

62. WHAT IS THE ROLE OF CORTICOSTEROIDS?
 The only two clinical indications for which the use
of corticosteroids has been demonstrated to
improve the outcome are TB meningitis and
pericardial TB
 Intriguingly, the benefit is evident in terms of
mortality only
 It seems unlikely that corticosteroids would be
able to reduce the development of complications
such as ureteric obstruction in patients with
GUTB. This issue is worth investigating

63. EVALUATION OF A PATIENT WITH GUTB -
A PHYSICIAN’S PERSPECTIVE
 All patients with GUTB should be evaluated for concomitant involvement of the lungs
as well as other organs
 Review of symptoms such as cough, expectoration, hemoptysis, and dyspnea
followed by a chest radiograph and examination of at least three sputum-smears for
acid-fast bacilli is the minimum evaluation for pulmonary involvement required in all
patients with GUTB
 Patients should be meticulously questioned about treatment for TB in the past for a
period more than one month
 If present, the chances of drugresistant TB are higher, and Category II DOTS would
be the appropriate treatment
 In India, about 5.2% of patients with TB have underlying HIV co-infection and extra-
pulmonary involvement occurs more commonly among HIV co-infected patients
 All patients should therefore be offered voluntary counseling and testing services for
detecting HIV co-infection

64.  The most common reason for planned treatment
interruption is the development of drug-induced
hepatotoxicity
 Old age, malnutrition, hypoalbuminemia, and alcoholism
are associated with increased risk of drug-induced
hepatotoxicity
 All patients should have their liver function evaluated before
initiation of treatment
 Liver functions have to be periodically monitored in patients
with preexisting liver disease, abnormal liver function at
baseline, alcoholics, and those developing symptoms
suggestive of drug-induced hepatotoxicity such as anorexia,

65. APPROACH TO A PATIENT WITH UNRESPONSIVE
DISEASE
 A patient with GUTB or any other form of TB
who fails to show improvement with treatment,
of symptoms or lesions evident on imaging, is a
commonly encountered situation in clinical
practice
 The following possibilities need to be
considered - Is the regimen and dosage of
drugs correct? Is the patient adherent? Was the
diagnosis of Tb correct? Is it drug-resistant TB?

66.  When all these possibilities have been
reasonably excluded, the most likely
explanation would be a delayed response to
treatment which is a common phenomenon in
extrapulmonary TB

67. SURGICAL MANAGEMENT OF RENAL
TUBERCULOSIS
 In a patient with unexplained LUTS, urinary T B
should be ruled out, as Chang had said, .The
kidney is an inarticulate organ; its vocal cords are
the bladder..
 Tuberculosis is a great imitator of other diseases
and can present as vague symptoms
 The patients should be managed based on clinical
and radiological findings
 All patients with active or latent urinary TB require
treatment with anti-TB chemotherapy

68.  The invasive or operative procedures for renal and ureteral TB can
be categorized into the following groups:
(1) drainage for hydronephrosis (ureteric stenting or percutaneous
nephrostomy);
(2) drainage of abscesses or localized collections;
(3) definitive local treatment of the affected part of the kidney
(cavernotomy/partial nephrectomy);
(4) nephrectomy of the non-functioning tuberculous kidney
(open/laparoscopic/ retro-peritoneoscopic techniques) and
(5) Reconstruction of the upper urinary tract (uretero calycostomy,
ureteric reimplantation, ileal ureteric replacement)

69. DOUBLE-J (DJ) STENTING
 It is common in tuberculous kidneys to observe
hydronephrosis secondary to stricture involving
the pelvi-ureteric junction or the ureter
 As these lesions heal by fibrosis, further
worsening of the stricture can occur with
treatment
 A DJ stenting of the affected system will help in
restoration of the patency of the drainage
system

70.  It facilitates a passive dilatation of the ureter and
prevents any further worsening by acting as a
splint across the site of stricture
 The strictures should be monitored with CT or
IVU
 If there is deterioration or no improvement after
a six-week period, then surgical reimplantation
or other minimally invasive procedures including
balloon dilatation may be necessary

71. PERCUTANEOUS NEPHROSTOMY
 Many patients have multipleinfundibular stenoses with
individual calyces being dilated and non-communicating
with each other
 There may be a further deterioration of the renal function
with chemotherapy, as the calyx may be cut off from the
rest of the collecting system secondary to fibrosis
 DJ stenting may not be effective in such circumstances,
as the individual calyces do not communicate with each
other
 In such instances, a percutaneous nephrostomy, if
required multiple, may be necessary, in order to protect

73. CAVERNOTOMY:
 Sometimes the lesions are characterized by extensive
cavitations, which usually occur at the poles of the
kidney
 The involved calyces do not excrete contrast medium,
making it difficult to make a diagnosis of the condition
 It is extremely important to have an index of suspicion in
these patients, as large conglomerated, non-
communicating tuberculoma formed because of
infundibular stenosis may radiologically mimic a renal
tumor
 Ultrasound or CT abdomen usually helps us diagnose

74.  In view of ischemia to that particular segment of the
kidney, the drugs may not reach the desired therapeutic
levels, resulting in a persistence of the lesion even after
the completion of the course of chemotherapy
 When patients do not respond to medical therapy or if
the disease process has gone unnoticed, the cavity
containing urine may be secondarily infected to form an
abscess
 Previously, cavernotomy was considered an ideal option.
With the advent of Pyrazinamide, which acts
intracellularly, and with the availability of better imaging
modalities, this procedure hardly has any place in the
modern era of management

75. PARTIAL NEPHRECTOMY
 Caution should be exercised if there is a calcification in
the wall, as slow but insidious extension of the
calcification might ultimately destroy the whole kidney
 Once this process starts, it is advisable to consider
partial nephrectomy
 There are only two indications for
 partial nephrectomy:
(1) a localized polar lesion containing calcification that has
failed to respond after six weeks of intensive
chemotherapy;
(2) an area of calcification that is slowly increasing in size
and threatening to gradually destroy the entire kidney

76. CALYCORRHAPHY/INFUNDIBULOPLASTY
 The non-communication of the cavity with the rest
of the system necessitates a closer follow-up and
if the calyx is functional may require a
calycorrhaphy or infundibuloplasty
 If the corresponding pole of the kidney is non-
functional, polar nephrectomy is advocated. In
patients with a cicatrized renal pelvis and ureter, it
may be necessary to perform a lateral
nephrotomy to open the infundibulum of all the
major calyces, replace the ureter with ileum, and
anastomose the proximal end of the ileum to the
lateral border of the cavity

77. NEPHRECTOMY
 Appearance of calcification in a tuberculous kidney is a
sign of advanced stage of the disease and is reported
in up to 50% of patients with renal tuberculosis
 When a tuberculous lesion has advanced to the
collecting tubules or the renal pelvis, it never heals
completely because of a hindered drainage and
backpressure effects
 When complete healing occurs with antituberculous
therapy, the tuberculous process usually is limited to
the cortex and has never extended to a pyramid or
collecting tubules

78.  The indications for nephrectomy in a non-
functional asymptomatic tuberculous kidney
are still debatable

79.  Fundamental principles while doing nephrectomy for a
non-functioning tuberculous kidney:
 It is preferable to approach the kidney from behind, as
the kidney is more often adherent to the colon anteriorly
in view of severe inflammation
 It is not necessary to remove the ureter completely as
the goal should be to remove as much of the diseased
ureter as possible
 Every effort should be taken to ligate the artery and the
vein separately, in order to prevent the possibility of
development of arterio-venous fistula if both are tied
together

80.  Before exploring a non-functioning tuberculous
kidney, it is important for the urologist to
consider certain issues:
(a) Is there a danger of viable tubercle bacilli in a
tuberculous kidney?
(b) Is salvage of a poorly functioning tuberculous
kidney always possible?

81.  Ideally, percutaneous nephrostomy is the best
method to assess the recoverability of renal
function
 It promptly decompresses the obstructed kidney
and helps to estimate the creatinine clearance of
the diverted urine
 The limitations are that it is an invasive procedure
and if the kidney is non-functioning, nephrectomy
has to be done in order to prevent the occurrence
of a nephro-cutaneous fistula

82.  On the other hand, if the patient.s GFR is <15
ml/min and the cortical thickness is <5 mm,
associated with more proximal lesions, it is a
more likely that the kidney is not worth
salvaging
 In such instances, it is better not to intervene,
as these kidneys are less likely to improve
after intervention

83. TUBERCULOSIS AND RENAL FAILURE
 Tuberculous infection is 6-16 times much more
frequent in patients undergoing hemodialysis
than in the general population
 Renal disease can be particularly occult and
insidious, leading to progressive destruction
and calcification of the parenchyma
 Renal TB can result in end-stage renal disease
by two mechanisms:
(1) it can inß ict direct insult to renal parenchyma
by causing obliterative endarteritis

84. of the intra-renal segmental vessels or secondary
renal amyloidosis
(2) by the obstruction of pelvi-ureteric junction or
multiple infundibular stenoses, it can result in
obstructive uropathy
 The overall incidence of renal failure reported in
the literature is 24%

85.  Renal TB can also result in certain biochemical
abnormalities in patients with end-stage renal disease
 Hypercalcemia is one such important biochemical
abnormality seen in such patients
 This usually occurs secondary to abnormal calcitriol
production by the granulomatous tissue
 This ectopic production of calcitriol by the granulomas
is either unregulated or is regulated by ways different
from those controlling the normal renal production of
this hormone

86.  Peces et al. reported that a successful management of
TB resulted in resolution of hypercalcemia and an
adequate parathyroid hormone response
 Any attempts at correction of hypercalcemia alone may
prove detrimental to these patients
 Patients with bilateral renal TB can present with acute
renal failure
 Conte et al. in their report suggested that any patient
with acute renal failure in whom no definite cause could
be identified, TB should be considered

87.  If the patient presents with obstructive
uropathy, it is necessary to do an initial
diversion in the form of percutaneous
nephrostomy and allow sufficient time for the
serum creatinine levels to reach a nadir value,
before planning any form of definitive
intervention
 In patients with renal failure requiring a bowel
interposition, a short ileal conduit is preferred

88.  Bowel interposition leads to various metabolic
abnormalities and already existing renal failure
could further worsen with time
 Such patients need to be closely followed up as
they could develop chronic renal failure
necessitating dialysis and renal transplantation

89. OPTIONS IN THE MANAGEMENT OF
TUBERCULOUS URETERIC STRICTURE
PATHOLOGY
 Site of stricture formation in decreasing order of frequency:
ureterovesical junction(mc)
ureteropelvic junction
middle third of the ureter
entire length of ureter
 The length of stricture varies, but lower ureteric strictures are usually
<5 cm in length
 While the circular fibrosis gives rise to strictures, the longitudinal
fibrosis leads to shortening of ureter, pulling up the orifice as a
gaping hole -the so-called golf hole
 Ureteric calcification, albeit a theoretical possibility, is rarely seen
clinically

90. DIAGNOSTIC WORKUP
 The specific investigations in a case of ureteric stricture
are principally aimed at defining:
a. the site, extent, number, and caliber of stricture,
b. defining the degree and impact of backpressure
changes and/or coassociated tuberculous disease on
renal function
c. defining the extent of involvement of urinary bladder
and contralateral unit, and
d. defining extent of tuberculous involvement in the
segment of bowel which may be required for ureteric
replacement

91. TREATMENT
 Once the diagnosis of urinary TB is confirmed
on investigations, the patients should be put on
multidrug antituberculous drugs (ATT).
 Any intervention should be done after the
patient has received at least 4-6 weeks of ATT

92. TREATMENT IN EARLY DISEASE
 When the investigations show early ureteric
disease, every attempt should be made to
place a DJ stent. If DJ stent placement is not
done, these patients should be followed
closely with monthly limited film IVU or renal
scan
 If there is no improvement or deterioration for 6
weeks then early intervention (DJ stenting or
Percutaneous nephrostomy (PCN)) has to be

93.  The patients of tuberculous ureteric stricture
may be grouped into two broad categories:
I. Simple/uncomplicated: Short segment
passable stricture with salvageable renal
function and good bladder capacity
II. Complex/complicated: Long segment,
extensive/bilateral, or impassable stricture with
or without salvageable kidney and bladder

94. ENDOUROLOGIC OPTIONS FOR
MANAGEMENT OF URETERIC STRICTURE
Double-J stent placement:
 DJ stent placement also gives the best outcome if
the ureteric stricture is short and not dense with a
functioning renal unit and with reasonable bladder
capacity
 Subsequently, this stent can be replaced with a
larger size stent
 The stent can be kept for a period of 6-12 months
and usually by that time the stricture stabilizes

95.  This technique is rarely definitive and usually
requires repeated dilatations on a regular basis
 The dilatation is repeated every 2 weeks initially,
later every 1-2 months, until the upper renal tract
has stabilized
 Contraindications include active infection and
length of stricture more than 2 cm, because
dilatation alone will rarely be successful in this

96. Antegrade balloon dilation
 If retrograde access fails, antegrade approach
may be attempted particularly if the patient
already has nephrostomy in situ

97. Endoureterotomy:
 Like balloon dilation, this procedure can be done either
through the retrograde or the antegrade approach
Cautery wire balloon incision
 This procedure is performed under fluoroscopic control
 This procedure is not advocated when the stricture is in
close proximity of great vessels, such as at the iliac level of
the ureter
 The favorable prognostic features were: length of stricture
<1.5 cm, nonischemic nature of stricture, and adequate
renal function

98. SURGICAL OPTION IN MANAGEMENT OF
TUBERCULOUS STRICTURE
 When endourologic treatment fails
Ureteroureterostomy
 A short defect involving the upper or midureter can be
treated by ureteroureterostomy.
 The anastomosis should be tension-free, hence enough
ureteral mobility is essential prerequisite
Ureteropyelostomy/ureterocalicostomy
Psoas hitch: If the bladder capacity is normal, psoas hitch
can be performed for small length strictures of the lower

99. Boari flap:
 If the bladder capacity is normal, Boari flap may
be employed for long lower ureteric stricture
Intubated ureterotomy:
 This procedure was popular for long upper and
mid-ureteric strictures wherein the incised ureter
was left to heal by regeneration over a stent
Transureteroureterostomy:
 if the other ureter is also diseased this should be
attempted with caution

100. Ileal ureteral substitution
 For long ureteric strictures involving almost the
whole length of ureter or upper ureteric
strictures require ileal replacement of ureter
 The contraindications -baseline renal
sufficiency with serum creatinine value of >2
mg/dl
 An isoperistaltic segment of ileum is used and
the lumen can reduced by tailoring

101. Autotransplantation
 For proximal or multiple/pan ureteric strictures
when other methods of repair fail or are not
feasible, autotransplantation is an option

102. RECONSTRUCTIVE BLADDER SURGERY IN
GENITOURINARY TUBERCULOSIS
There are two types of lesions in the tubercular bladder:
 One, which is more common, is when the bladder due to
active infection has a reduced capacity of about 150-200 ml
 The other type is the true or structural bladder contracture
wherein the urinary bladder has permanently lost its
capacity and has little or no value as a urinary reservoir
 In the initial stages before cicatrisation has taken place, the
dome contracts but the trigone and bladder neck are
relatively spared
 Antitubercular therapy is often successful in preventing
disease progression and restoring normal bladder function

103.  But once the tubercular bladder shrinks to a very small
size (reduced elasticity and compliance) - tubercular
thimble bladder - the process may no longer be
reversible and corrective(reconstructive) surgery in the
form of augmentation must be performed to
prevent/arrest kidney damage
 The aims of the reconstructive surgery are –
(1) Enlargement of the small urinary bladder to enable the
patient to retain urine for a reasonable period of time
(2) restoration of function as a low-pressure (less than 30
cm of water) reservoir during storage and as a high-
pressure compressor during micturition

104. (3) prevention of incontinence and infection that may
jeopardize upper urinary tract integrity
 Before any surgical intervention, a minimum of four
weeks of ATT is recommended, which allows
1. stabilization of the lesion and better planning of
reconstructive surgery
2. recovery of renal function in patient, if adequate
temporary urinary diversion is provided.

105. SURGICAL OPTIONS:
 AUGMENTATION CYSTOPLASTY
 SIGMOIDOCYSTOPLASTY (COLOCYSTOPLASTY)
 ILEOCYSTOPLASTY
 CAECOCYSTOPLASTY
 ILEOCAECOCYSTOPLASTY
 GASTROCYSTOPLASTY
 ORTHOTOPIC NEOBLADDER

106. REPRODUCTIVE TRACT TUBERCULOSIS AND
MALE INFERTILITY- MANAGEMENT
 The primary aim is to treat the infection and
requires antitubercular therapy(Rarely, in patients
with an early diagnosis of the disease who have
not developed bulky granulomas causing an
obstruction, this therapy may result in restoration
of fertility)
 In the majority of cases, the presentation is late
and antitubercular therapy does not improve the
fertility status
 Infertility here usually results from anatomic
obstruction and therapy depends on the site and

107. Ejaculatory duct obstruction
 While the diffuse, fibrotic type of lesions of the
ejaculatory duct and seminal vesicles- not amenable to
surgery
 patients with discrete obstructions at the distal end of the
ejaculatory duct - TURED or TUIRED
Epididymal obstruction
 Patients with palpable masses usually require excision
of the epididymis, both for diagnosis and therapy of
tuberculosis,precluding surgical reconstruction in most
cases

108.  Patients who have obstructive azoospermia with normal
volume, fructose-positive ejaculate-discrete obstruction
either within the vas deferens or at the vaso-epididymal
junction-microsurgical reconstruction(vasovasal
anastomosis or vasoepididymal anastomosis)
Assisted reproduction
 Patients who are not amenable for surgical correction
 Choices:
1. in-vitro fertilization or
2. Intracytoplasmic sperm injection (ICSI)
 results comparable to those in men without this disease

109. TUBERCULOSIS IN RENAL TRANSPLANT
RECIPIENTS
 The reported prevalence of post transplant TB-
Asia -3.1 to 15%
South Africa -1.5 to 8.5%,
Middle East- 1.5 to 3.5%
Europe -1.7 to 5%
United States- 1.5%
 About 45-60% of TB occurs in the first year after
transplantation
 An earlier occurrence was noted with non-renal solid organ
transplantation, cyclosporine, anti CD3 therapy, malnutrition
secondary to prolonged dialysis, relative immunodeficiency
and exposure to the organism in hospital setting

110. The major risk factors for TB are:
 chronic liver disease (2times)
 other coexisting infections
 particularly deep mycoses
 pneumocystis pneumonia
 nocardia (1.6 times)
 OKT3 (1.8 times)
 CMV infections (2.25 times)
 Cyclosporine use advances the onset to an earlier
date andpatients on cyclosporine seldom develop
TB later than six years

111.  The presentation of the disease differs in solid
organ recipients and a high index of suspicion is
important in diagnosing the problem
 Rifampicin, a vital drug in the ATT regimen
induces cytochrome-c P450 microsomal enzyme
system which is responsible for metabolizing
cyclosporine, sirolimus and prednisolone
 This unpredictable interaction has led to acute
rejections in 30% and graft loss is 20% and hence
rifampicin should be avoided in solid organ
transplantation
 The dose of calcineurin inhibitors may have to be
increased two- to fivefold to overcome this effect

112. Duration of therapy:
 The regimens used in different centers vary in
dose and duration which are not validated
 authors use a four drug regimen:
 pyrazinamide (3months);
 ofloxacin (9 months);
 INH and ethambutol (18 months)
 If rifampicin has to be used for those who are not
on cyclosporine, prednisolone dose has to be
doubled

113.  Drug resistance and atypical mycobacterial
infections are emerging problems and should
be suspected in the non-responding patients