The document discusses the development of the urinary system from the intermediate mesoderm. It describes the development of the pronephros, mesonephros, and metanephros, as well as the ureteric bud and metanephric blastema that form the definitive kidney. It also discusses imaging in urinary tract tuberculosis, noting that the intravenous urogram remains the gold standard for imaging early renal TB while plain radiography can identify calcification. Pathogenesis involves hematogenous spread from a primary focus that can reactivate if immunity breaks down, causing renal parenchymal and pelvicalyceal changes through competing destructive and healing processes.

1. Presenter : Dr. Bidyut Debnath
Moderator: Dr.(Prof. ) B. K. Duara
Development of the urinary system and
Imaging in Urinary Tract Tuberculosis

2. Development of the kidney
The kidneys develop from
a mesodermal ridge
known as the intermediate
plate mesoderm, which
develops lateral to the
paraxial mesoderm, along
the posterior wall of the
abdominal cavity.

4. *During intrauetrine life, the
intermediate mesoderm is
organised into three
overlapping kidney systems
in a cranial to caudal
direction
Pronephros
Mesonephros
Metanephros.

5. THE PRONEPHROS
Derived from the intermediate
mesoderm in the cervical
region
It forms vestigial excretory
units, the nephrotomes, that
regress eventually.
By end of fourth week, all
evidence of pronephros
disappears.

6. THE MESONEPHROS
The Mesonephros and Mesonephric ducts are derived from the
intermediate mesoderm in the upper thoracic to lumbar L3 region.
• In the 4th
week, during regression of the pronephros system, the first
excretory tubules of the mesonephros appears.
• The mesonephric ducts become functional between 6 to 10 weeks.
• By the end of the second month, majority of the tubules have
disappeared.
• Mesonephric duct remains in males for the formation of the genital
system.
• In female they regress.

7. URETERIC BUD
A ureteric bud arises off
the mesonephric duct by 28
days.
This ureteric bud will
connect with the
metanephric blastema by
32 days.

11. THE METANEPHROS : THE DEFINITIVE
KIDNEY
The permanent kidney develops
from two sources :
The collecting system from the
ureteric bud
The excretory system from the
metanephric blastema.

12. *Collecting system :
The ureteric bud penetrates the
metanephric tissue. Subsequently
the bud dilates forming the
primitive renal pelvis and splits
into cranial and caudal portions,
the future major calyces.
Each calyx forms two new buds
and each bud will subdivide until
12 or more generations of
tubules have formed.
Thus the ureteric bud gives rise
to the ureters,renal pelvis, the
major and minor calyces, and
approximately 1 to 3 million
collecting tubules.

14.  The excretory system :
 Develop from the metanephric mesoderm
derived from the posterior intermediate
mesoderm.
 The ureteric bud induces mesenchyme to form
an epithelial aggregate, a metanephric tissue
cap. Under the influence of the tubule, cells of
the tissue cap form small vesciles, the renal
vesciles, which in turn give rise to small S-
shaped tubules.
 Capillaries grow at one end of the tubules
differentiating into glomeruli which will indent
into the proximal end of these tubules forming
the Bowman’s capsule.The distal end will
come in connection with the collecting
tubules. Rest of the tubule will form the
proximal convoluted tubule, loop of Henle and
distal convoluted tubule.

16. Phenomenon of Reciprocal Induction
Ureteric bud induces the formation of the tubules in the
metanephric blastema while the blastema induces the
development of the ureteric bud.

17. ASCENT OF THE KIDNEY
The kidney is initially in the pelvic region, later migrates to a
more cranial position in the abdomen during the 4th
to 8th
week of
gestation.
Ascent is actually caused by diminution of the body curvature and
by differential growth of the body in the lumbo-sacral region.
At the same time, the kidneys rotate 90 degrees medially such that
the renal pelvis comes to lie anteromedially.
In the pelvis, blood supply is from lateral sacral branches of the
aorta. As it ascends it is supplied by continuously higher levels of
branches from the aorta upto definitive renal arteries at L1 –L2.

20. Developmental Abnormalities of kidney
1.Renal dysplasias and agenesis: A spectrum of severe malformations that
represent the primary diseases requiring dialysis and transplantation in the first
years of life.
o Multicystic dysplastic kidney- Numerous ducts are surrounded by
undifferentiated cells. Nephrons fail to develop and the ureteric bud fails to
branch, so that the collecting ducts never form.
o In some cases these defects cause involution of the kidneys and renal
agenesis. Renal agenesis may also occur if the ureteric bud fails to contact
and/or induce the metanephric mesoderm.

21. 2.Congenital polycystic kidney: Numerous cysts form.
ºAutosomal recessive polycystic kidney disease,
which occurs in 1/5,000 births, is a progressive disorder in which cysts
form from collecting ducts. The kidneys become very large, and renal failure
occurs in infancy or childhood.
ºAutosomal dominant polycystic kidney disease,
cysts form from all segments of the nephron
and usually do not cause renal failure until
adulthood. The autosomal dominant disease
is more common (1/500 to 1/1,000 births)
but less progressive than the autosomal
recessive disease.

22. 3.Duplication of the ureter:
Results from early splitting of the
ureteric bud. Splitting may be
partial or complete, and
metanephric tissue may
be divided into two parts, each with
its own renal pelvis and ureter.
More frequently,
however, the two parts have a
number of lobes in common as a
result
of intermingling of collecting
tubules. In rare cases one ureter
opens into the
bladder, and the other is ectopic,
entering the vagina, urethra, or
vestibule

23. Abnormal Location of the Kidneys
During their ascent the kidneys pass through the arterial fork formed by the
umbilical arteries, but occasionally one of them fails to do so. Remaining in
the pelvis close to the common iliac artery, it is known as a pelvic kidney.
Sometimes the kidneys are pushed so close together during their passage
through the arterial fork that the lower poles fuse, forming a horseshoe kidney.
The horseshoe kidney is usually at the level of the lower lumbar vertebrae, since
its ascent is prevented by the root of the inferior mesenteric artery.

24. DEVELOPMENT OF THE URINARY BLADDER
AND URETHRA
 The caudal end of the hindgut is lined with endoderm and is known as the
cloaca. During the fourth to seventh weeks of development, the cloaca is
divided by a wedge of mesenchyme, the uro-rectal septum, into the uro-genital
sinus anteriorly and anal canal posteriorly.
 the uro-genital sinus may be divided into three component parts.
 The first of these is the cranial portion which is continuous with the allantois
and forms the bladder proper.
 The pelvic part of the sinus forms the prostatic urethra and membranous
urethra in the male and the membranous urethra and part of the vagina in
females.
 Thirdly, the caudal portion, or definitive uro-genital sinus, forms the penile
urethra in males and the vestibule in females.

27. TRIGONE PORTION

28. Bladder Defects
º When the lumen of the intraembryonic portion of the allantois persists, a
urachal fistula may cause urine to drain from the umbilicus.
º If only a local area of the allantois persists, secretory activity of its lining results
in a cystic dilation, a urachal cyst.
º When the lumen in the upper part persists, it forms a urachal sinus.

29. º Exstrophy of the bladder: A ventral body wall defect in which the bladder
mucosa is exposed. Epispadias is a constant feature and the open urinary tract
extends along the dorsal aspect of the penis through the bladder to the
umbilicus.
May be caused by a lack of mesodermal migration into the region between
the umbilicus and genital tubercle, followed by rupture of the thin layer of
ectoderm. This anomaly is rare, occurring in 2/100,000 live births.

30. Imaging in Urinary Tract
Tuberculosis

31. oTuberculosis (TB), is the commonest worldwide cause of mortality from
infectious diseases with nine million new cases and two million fatalities per year.
o Approximately 95% of cases occur in developing countries.
oIn India, more than 1000 lives are lost every day due to TB despite
the availability of modern diagnostic aids and treatment.
oThe genitourinary tract is a primary target of hematogenous infections and is the
most common site of extra pulmonary TB, comprising 14 41% of the same.‑ ‑
oGenitourinary tuberculosis (GUTB), a term coined by Wildbolz in 1937.
oWorldwide, 15% of TB patients are co infected with HIV, and in HIV endemic‑ ‑
areas, as many as 75% of patients with GUTB are co infected with HIV.‑
Introduction

32. Patient Population
o GUTB usually affects adults between the second and fourth decades of life.
o Rare in children and in the fifth and sixth decades.
o Mean age 40.7 years (range: 5 90 years)‑
o Long latent period (5 40 years) between the original pulmonary infection and‑
the appearance of clinical renal Disease*.
oThe youngest reported case of UTB was 2 years old.
oIn India, it is not uncommon to see children with UTB.
TB autonephrectomy has been seen in a six year old girl.

33. Clinical Details
oInsidious onset
oNo specific symptoms
oAtypical presentations
} which lead to difficulty and delay in diagnosis
oLocal symptoms :Most common
 frequent voiding
Dysuria
Pyuria
back, flank, or abdominal pain
microscopic or macroscopic hematuria
oSystemic symptoms :Less common
Fever
weight loss
anorexia
 Hematuria and culture negative pyuria may be seen at urine analysis.‑

34. Pathogenesis
Causative organisms
Mycobacterium tuberculosis, an obligate pathogen, is the usual cause
Mycobacterium bovis
Mycobacterium avium intracellulare (MAIC)
Spread of tuberculosis to the urinary tract
 Hematogenous dissemination: from a primary TB focus within the lungs, bone,
or other organs
Bacille Calmette Guerin (BCG): a live vaccine strain can cause renal lesions via‑
reflux, in 0.1% of patients undergoing intravesical instillation of BCG for
the treatment of bladder cancer

35. Spread of infection at the time of primary tuberculosis
primary infection(Lung)

alveolar macrophages
phagocytose one or more
mycobacteria lodged within
an alveolus

mycobacteria multiply
within the macrophages
lymphatic and
hematogenous dissemination
And seeding of tubercular
bacilli throughout the body

The kidneys, and possibly the prostate and seminal
vesicles, are often the primary sites of GUTB.
 All other uro-genital organs, including the epididymis
and bladder, become involved by ascent or descent of
MTB from a source elsewhere in the genitourinary tract

36. In most patients, acquired cellular immunity develops and there is inhibition of
bacterial multiplication and containment of the disease by the formation of
microscopic granulomas.
In immune competent patients, these granulomas heal or remain stable for‑
many years.
If there is a breakdown in host immunity, re activation or re infection occurs. It‑ ‑
has been reported that a reduction in serum 25 OH vitamin D levels leads to fall‑ ‑
in cell mediated immune defenses, which can result in activation of latent‑
tuberculosis.

37. Renal Parenchymal changes
o Reactivation occurs at the corticomedullary junction.The medullary portion of the renal
parenchyma is usually spared initially.
oCortical granulomas enlarge and coalesce, with the bacilli spilling down the nephrons and
getting trapped in the narrow segment of the loop of Henle, establishing new foci of
infection within the renal pyramid.
o These papillary lesions caseate and cavitate, frequently forming ulcero cavernous‑
lesions as they erode into the pelvicalyceal system (PCS).
o Extensive papillary necrosis may develop with the formation of frank cavities and
destruction of the adjacent renal parenchyma.
o These may also extend into the collecting system via rupture, or cause parts of the
papillae to become necrotic and slough.
o A mass lesion may result from massive destruction and coalescence of granulomas, if
they do not rupture into the adjoining calyx.Alternatively, these granulomas may coalesce
and form cavities after liquefaction.
o Hypercalcemia may occur, usually secondary to abnormal cortisol production by
granulomatous tissue.

38. Pelvicalyceal system and Ureteric changes
o When bacilli are shed into the urine, the disease spreads antegradely to involve
the urothelium of the renal pelvis, ureter, bladder and, at times, the adjacent
genital tract.
o Infection in the walls of the calyces, pelvis, and ureter produces significant
inflammatory mucosal thickening. Microscopic granulomas may form here too.
Ulceration soon follows.
o In advanced disease, in addition to loss of parenchyma by caseation, intra renal‑
scars and strictures lead to obstruction and dilatation of segments of the PCS.
Strictures are more common at sites of normal narrowing, such as the calyceal
neck, the pelvi ureteric junction, and the ureterovesical junction.‑
o Obstruction may lead to massive hydronephrosis or hydrocalicosis which may
be the final stage.

39. TB of the kidney thus reflects competing processes:
(a)The destructive effects of the bacilli, leading to ulceration, cavitation, and
fistulization
(b) the host’s secondary defense and healing mechanism leading to the
formation of granulomas along with fibrosis, calcium deposition, and strictures,
which may worsen the obstruction causing progressive renal dysfunction.
However, both processes occur concurrently and may lead to a
non functioning, calcified kidney of any size; this process is called‑
autonephrectomy. Nephrectomy has been advised to remove the trapped
dormant bacilli in such autonephrectomized kidneys.

40. Tuberculous interstitial nephritis (TIN)
Occasionally, TB can affect the kidney more insidiously, causing TIN, which, if
untreated, progresses to renal failure. Rupture of the bacilli into the
interstitium can lead to isolated interstitial disease, without persistent
pyuria, hematuria, or identifiable AFB in the urine, leading to diagnostic
dilemmas.

41. Changes In Urinary Bladder
o It produces irregular mural thickening which subsequently proceeds to fibrosis.
oThis results in reduction in the bladder capacity and may obstruct the ureters.
oAlternatively, traction on the ureteric orifices may lead to vesicouretcric reflux.
oCalcification (10% )
Urethral TB is very rare despite the constant exposure of the urethra to the
infected urine. Most often it occur in association with upper tract involvement.
Isolated urethral involvement is extremely uncommon. Tuberculosis of the urethra
is usually due to the spread from another focus in the genitourinary tract, the
prostate being the common source.

47. MODALITIES FOR IMAGING
 PLAIN RADIOGRAPH
 IVU STUDY
 RGU MCU
 USG AND DOPPLER STUDY
 CT SCAN
 M R I
 RENAL SCINTIGRAPHY
 The intravenous urogram (IVU)
remains the gold standard in
imaging early renal TB.

48. The plain radiograph
Identification Urinary tract of calcification
Signs of active or inactive extrarenal tuberculosis (such as osseous or paraspinal
changes of tuberculosis, as well as old, healed, calcified splenic, hepatic, lymph node,
and adrenal granulomas) may be apparent
 Patterns varies from few minute areas of calcification to a complete cast of
the kidney
o Initially :faint and punctate, may be amorphous, granular, or curvilinear.
o Later :
 Focal globular calcification involving a renal lobe is frequently associated
with a granulomatous mass.
 Triangular ring like‑ calcifications that are characteristic of papillary
Necrosis.
 ‘Putty kidney’ - Homogeneous and moderately dense, with ground glass
appearance (Due to Calcified caseous tissue)

49. Plain radiograph of the abdomen in a
woman with renal tuberculosis shows
calcification of varying patterns
(curvilinear, amorphous, speckled).

50. Classic lobar pattern of calcification, which is pathognomonic of end-stage renal
tuberculosis, with Ureteral calcification , which is fainter in upper parts.
The occurrence of any upper ureteral calcification (however, faint) along with any other renal
calcification is a good pointer of renal TB.

51. Intravenous urography
Early changes:
o Minimal calyceal dilatation(Earliest) and mild loss of calyceal sharpness due to
mucosal edema.
o As the disease progresses, the calyceal outline becomes more irregular, fuzzy,
and ragged and, later, feathery and moth eaten in appearance.‑
o Papillary necrosis,
o Initial cavitation
Late Changes:
oExtensive cavitation
oFibrotic strictures
oCortical scars
oMass lesions
oCalcification
oAutonephrectomy
oPerinephric abscess
oFistula formation.
The finding of hydrocalyces with no pelvis
dilatation or an atrophic pelvis is highly
suspicious for tuberculosis

52. A.lower infundibular and
renal pelvic
scarring,papillary
necrosis
B.papillary necrosis in the upper
group of calyces,
Healing forniceal papillary
necrosis in a lower calyx
C.multiple parenchymal cavities with areas of
papillary necrosis

53. o The cephalic retraction of
the inferior medial margin
of the renal pelvis at the
ureteropelvic junction
(UPJ), or the "hiked up
renal pelvis, is another
suggestive urographic
change.
.

59. Autonephrectomy
The late phase of progression of granulomatous destruction of the kidney, with
subsequent obstructive uropathy, can lead to an autonephrectomy. This is
considered typical of end stage renal TB.‑
There are two types:
(1) the caseo cavernous autonephrectomized kidney, i.e., an enlarged kidney‑
converted into a caseous filled sac, with or without calcification.
(2) the shrunken, fibrotic, and often calcified kidney. In both instances, there is
usually obstruction of the ureter at some point, but this is not essential in type (1).
However, both types will be non functional on the IVU‑

63. False positives/negatives
 Renal calcification may occur in nephrocalcinosis, which has several causes.
Renal hydatid cysts, renal abscesses, and renal artery aneurysms may calcify
and mimic renal tuberculosis.
 Calcification may occur within bladder tumors, or calcium may be encrusted
on the surface of bladder tumors, which need to be differentiated from bladder
tuberculosis. A shrunken bladder may be neurogenic, but the clinical
presentation is not that of urinary tuberculosis.
 Ureteric and Bladder calcification more commonly occurs in patients with
schistosomiasis.
o In schistosomiasis, calcification is first observed in the bladder and then extends
upwars to the ureter. In contrast to tuberculosis, bladder capacity and contractility
are surprisingly well preserved.
Appeared as eggshell or linear areas of calcification in the submucosa of the bladder
and the distal
ureters
o In tuberculosis, calcification is more amorphous and patchy, and it extends down
the ureter

66. Sonographic features :
o Focal renal lesion–the parenchymal Granuloma / masses
o Cavities
o Urothelial thickening
o Focal caliectasis and Hydronephrosis
o Calcifications
o Renal Abcess and Perinephric Abcess
o Small and fibrotic thick walled bladder
o Echogenic foci or calification (Granulomas) in bladder wall near
ureteric orifice
USG and Doppler Study
Also Used for USG Guided FNAC

67. Granuloma The most frequently encountered sonographic
parenchymal abnormality
Small (5 15 mm)‑
º Echogenic
º have an echogenic border with a central area
of low echogenicity
Granulomas can be better appreciated on color flow imaging, as the
‘cut off’ of the vasculature.
Larger(>15 mm)
º Have mixed echogenicity and poorly defined
borders

68. Caseation occurring within the masses parenchymal cavities

69. Papillary
involvement may be
seen as an echogenic
non shadowing‑
medullary mass in
close proximity to the
calyces, into which it
commonly ruptures,
to produce a
cavitatory lesion that
communicates with a
calyx via a thin
or wide anechoic
tract.

70. Infundibular stenosis
Focal caliectasis
Urothelial thickening with
varying degrees of fibrosis
Obstruction affecting different sites
Uneven caliectasis
When the renal pelvis and ureter are involved
by TB, the hydronephrosis
becomes severe.
This pattern of diffuse uneven caliectasis
(without renal pelvic dilatation) accompanied
by urothelial thickening, is
a good pointer of renal TB, especially
in the absence of a renal pelvic calculus.

72. A TB renal abscess may be noted as an irregular
sonolucent cavity, with a semi solid echogenicity and a thick‑
ill defined wall. Necrotic debris and scattered echogenic foci‑
may be noted. The renal abscess can extend outward and
rupture, leading to a perinephric abscess and later to a
cutaneous fistula.
A thorough analysis of the retroperitoneal compartments
and, in particular, the psoas muscle sheath, is required as
these are possible sites of a migrating abscess.

73. Small and fibrotic thick walled bladder

74. USG is less sensitive than CT in detection of
oCalyceal, pelvic or ureteral abnormalities
oIsoehoic parenhymal masses
oSmall Calification
oSmall cavities that communiate with collecting system

75. CT Scan
Advantage:
o CT does not require bowel preparation.
o It directly visualizes the renal parenchyma, irrespective of renal function.
o Assesses extrarenal spread of the disease.
o CT is also useful in identifying renal scars, mass lesions, and urothelial
thickening.
o CT can also substitute for RGU in cases of a tight stricture.
o CT can detect calcification with greater accuracy, precision, and sensitivity
and is the most sensitive modality for identifying renal calcifications.
MDCT with contrast administration also allows dynamic
assessment of the kidney in different phases of excretion and
can define the extent of the disease and identify significant
obstruction as well as other complications

76. Early changes
Papillary necrosis
These can be appreciated on the
current high end MDCT scanners‑
 Solid mass with little or minimal enhancement after contrast
administration.
 The lesions can occasionally grow to a very large Size and may
form masses of mixed density due to the presence of areas of
calcification.
 Coalesced cortical granulomas containing caseous or calcified
material can be easily identified on CT.
Granulomas (≤3 mm)
Renal parenchymal changes
In rare cases, there may be single or multiple parenchymal nodules,
without collecting system involvement.The nodules are
variable sized, well defined parenchymal lesions on cross sectional‑ ‑ ‑
images and may mimic renal neoplasms, which may lead to
unnecessary surgery; these are therefore labeled as the
‘Pseudo tumoral’ Type.‑

78. oTubercular renal abscesses are seen as hypodense areas of 10 40 HU with‑
mild peripheral enhancement.

79. o Cavitation within the renal parenchyma may be seen as irregular pools of
contrast material if a calyceal communication exists.
Inflammatory granulomatous and caseating masses show enhancement.

80. o Healing leads to fibrosis and calcification.Fibrosis

81.  Fine calcifications are best seen on CT and may be good clues to the
presence of TB.
 Varies in appearance depending upon the stage and severity of the
disease from punctate, to amorphous, to thin rims surrounding
low attenuation areas of focal cortical inflammation ; to diffuse uniformly‑
radio dense areas, replacing part or all of the renal parenchyma, in‑
late stage disease.‑
The lobar pattern of calcification, which is pathognomonic for TB
Calcification

82. Pelvicalyceal system (PCS) and ureteral involvement
 Focal or diffuse caliectasis unaccompanied by renal pelvic dilatation.
 Urothelial thickening.
 Multifocal strictures lead to uneven caliectasis.
 Hydronephrosis
 Multiple ureteral strictures

83. With long standing renal TB, progressive parenchymal atrophy and‑
hydronephrosis lead to a loss of normal morphology, and the appearance
mimics multiple thin walled cysts or, occasionally, a multiloculated cyst‑

84. Calyces with Attenuation values if dilated with
 Fluid : 0 HU - 10 HU
 Debris and caseation :10 HU - 30 HU
 Putty like calcification : 50 HU to 120 HU‑
 Calculi :Greater than 120 HU

85. As destruction progresses, the dilated calyces are assimilated into the
caseous renal parenchyma and a unique ‘lobar caseation’ appearance is
recognizable. This can be easily differentiated from hydrocalycosis, as
each individual lobe does not connect to another as would be expected if
they were calyces

86.  Kenny stated that although pelvi infundibular strictures, papillary‑
necrosis, cortical low attenuating masses, scarring, and calcification may‑
be seen in other conditions, the combination of three or more of these
findings is highly suggestive of TB, even in the absence of documented
pulmonary disease.
 Three imaging patterns were described in CT of renal TB by Wang et al.
whenever multiple findings were noted:
(a) multiple stricture sites;
(b) a single stricture with one other imaging finding; and
(c) autonephrectomy along with any other imaging finding barring
stricture.
 The Lober pattern of calcification is pathognomonic of renal TB and
‘lobar caseation’ comes pretty close to the same.

87. MRI
 MRI provides good morphological details of the kidneys as well as
excellent delineation of the ureters.
 MRI is good at depicting tuberculous cavities, sinuses tracts, fistulous
communications, and extrarenal spread.
 MRI is also useful in the evaluation of peritonitis and adnexal masses.
 Renal parenchymal changes not dissimilar to acute pyelonephritis occur
in renal involvement with tuberculosis. Active inflammation may cause
focal tissue edema and vasoconstriction resulting in focal hypoperfusion
well depicted on MRI scans.
 Non contrast MRI is especially useful in patients with renal failure.‑

88.  MR urography (MRU) comprises an evolving group of techniques with the
potential for optimal non invasive evaluation of urinary tract abnormalities.‑
Both static fluid (non contrast, heavily T2W sequences) and excretory MRU‑ ‑
(performed during the excretory phase of enhancement after intravenous
gadolinium) can be combined with conventional MRI for comprehensive
evaluation of the urinary tract.
 Cine MRU demonstrates the ureters in their entirety and is useful for
confirming the presence of stenosis.
 Time resolved dynamic contrast enhanced MRU has been used in the‑ ‑
evaluation of ureteral peristalsis in GUTB.

89.  Clues indicating that the focal pyelonephritis has a tuberculous origin:
o Loss of interface between the infection and the adjacent renal parenchyma
o Surrounding tissue edema,
o Asymmetric perinephric fat stranding
o Thickening of Gerota’s fascia may be.
 A TB granuloma is seen as a solid mass of variable size.
o The smaller nodular lesions usually appear hypointense on both
T1W and T2W images
o Larger nodules may reveal central hyperintensity on T2W images.The
central T2 hyperintense signal is due to high numbers of macrophages, fibrosis,
and gliosis, as well as the increased lipid content, in these lesions.
 The necrotic debris along with the caseation and calcification results in a
heterogeneous hypo to iso intense signal on T2W images.‑ ‑
Caseation may have a slightly hyperintense appearance on T2W images.

96. RENAL SCINTIGRAPHY
 The role of radionuclides in imaging patients with renal tuberculosis is
confined to assessment of relative renal function by renography when
surgery or nephrectomy is contemplated.
 The agents used are technetium-99m (99mTc) diethylenetriamine
penta-acetic acid (DTPA), 99mTc mercaptotriglycylglycine (MAG-3), and
iodine-123 (123I) orthoiodohippurate (OIH).

97. Tc-99-DMSA(Dimercaptosuccinate)
 Uptake & retention of this radionuclide by renal tubules allows
visualization of the functioning renal cortical parenchyma
 Renal morphology-size, position, cortical scars, presence of calyceal
dilatation
Tc-99-DTPA(diethylene triaminepentacetic acid)
 Excreted solely by glomerular filtration, No tubular excretion or
metabolism
 Assessment of renal perfusion, GFR
 Due to its minimal retention by the renal cortex, visualization of the
cortex is less than optimal & is not the agent for evaluation of renal size
or morphology.

98. Tc-99-glucoheptone
 Combination agent- both some degree of renal cortical activity & excretion by
glomerular filteration.
 Major portion excreted by glomerular filteration while rest enters extracellular
space. Renal tubular uptake of protein bound fraction & is retained in renal
cortex for several hours.
I-131-Ortho iodo hippurate(Hippuran)
Tc-99-MAG3 (Mercaptoacetylglycylglycylglycine)