Renal Tuberculosis,classification ,staging, Radiology findings, X RAY,ULTRASONOGRAPHU,CT,MRI

2.  A subset of genitourinary tuberculosis,
accounts for 15-20% of extra-
pulmonary tuberculosis.
 Tuberculosis can involve both the renal
parenchyma and the collecting system
(calyces, renal pelvis, ureter, bladder and
urethra) and results in different clinical
presentations and radiographic
appearances.

3.  Clinical features are often non specific and
include:
 Dysuria;
 Pyuria;
 Back , flank pain or abdominal pain
 Microscopic or macroscopic haematuria
 Constitutional symptoms

4.  Renal infection results from Haematogenous Spread at the
time of primary infection, with multiple micro-abscesses
developing at the site of periglomerular capillary seeding.
 Normal Host Immunity is usually able to dampen the
disease with the usual development of a small inactive
granuloma.
 Usually there is a long latency between primary infection
and presentation which in most case occurs due to host
immunity becoming compromised.
 These quiescent granulomas then can reactivate, grow
and eventually communicate with the calyces, leading to
Downstream Infection.

8.  Both the renal parenchyma and the upper collecting
system (calyces and renal pelvis) can be involved. The
former is usually seen associated with the latter, which is
the most commonly involved site in the genitourinary tract.
 Infection limited to the renal parenchyma has two
morphological appearances :
 pyelonephritis
› appearances are similar to pyelonephritis caused by other
organisms
› hypoperfusion and swelling of all or part of the kidney
 pseudotumoural type
› single or multiple nodules
› mimics renal cell carcinoma

9.  Usually the collecting system is involved (either in isolation
or in combination with the parenchyma), and appearances
vary according to the stage of disease .
 early
› papillary necrosis (single or multiple) resulting in uneven
caliectasis
 progressive
› multifocal strictures and hydronephrosis
› mural thickening and enhancement (on cross-sectional
imaging)
 endstage
› progressive hydronephrosis and parenchymal thinning
› dystrophic calcification

10.  Plain film findings focus on calcification,
which is seen in 25-45%, at various stages
of disease.
 Triangular in papillary necrosis
 Focal or amorphous: putty kidney (endstage)

11. (a) Abdominal radiograph demonstrates extensive calcifications forming a cast of
the kidney and ureter.
(b) Photograph of the cut specimen shows complete replacement of the normal
kidney
by inflammatory debris

12. Plain radiograph
revealing classic lobar
pattern of
calcification, which is
pathognomonic of
end-stage renal
tuberculosis. Ureteral
calcification is also
noted

13.  Traditional plain film IVP is quite sensitive to renal
tuberculosis with only 10% of affected patients having
normal imaging. Features include:
 parenchymal scars 50%
 moth eaten calyces: early finding
 irregular caliectasis
 phantom calyx
 hydronephrosis
 Lower urinary tract signs (see bladder and ureteric
tuberculosis) also recognised include:
 Kerr kink
 sawtooth ureter
 pipe-stem ureter
 beaded or corkscrew ureter
 thimble bladder

14. Collimated image from intravenous urography
demonstrates
multiple papillary cavities.
Retrograde pyelogram shows that the upper
pole calix is stenotic (arrow) with associated
papillary necrosis.
The adjacent calix is fibrotic and distorted as

15. intravenous urogram revealing the ‘classic’ lobar pattern of
calcification in a non-functioning (R) kidney

16. (R) ureteric stricture (white arrow) with ureteric calcification (black arrowheads), pseudo-
calculi (black arrow), and irregular calcification in the parenchyma (circled area)

17. an upward pointing
(arrow) renal pelvic
calculus, suggesting
the presence of a
hiked up renal pelvis.
Multiple discrete
calcifications are
noted in an upper
polar tuberculosis
cavity (circled area)

18. (A) Intravenous urogram revealing lower infundibular (arrow) and renal pelvic scarring (curved arrow). Note areas
of papillary necrosis in the circled area, (B) Intravenous urogram revealing papillary necrosis in the upper group of
calyces, with irregularity of the calyceal margins and the lateral margin of the upper infundibulum (dotted circle),
indicating spread of infection from the calyx to the infundibulum. (Healing forniceal papillary necrosis of non-
tuberculosis origin noted in a lower calyx (arrow), (C) Intravenous urogram revealing multiple parenchymal cavities
(black arrows) with areas of papillary necrosis (white arrow) in the upper group calyces, bilaterally. The (L) upper
group (lateral division) calyceal outline is destroyed by adjacent granulomatous tissue (arrowheads)

19. Bilateral percutaneous
nephrostomogram revealing
multiple filling defects along the
upper ureter, bilaterally,
representing sumucosal
granulomas (empty
arrowheads). The large filling
defect noted in the (R) ureter is
a calculus (white arrow). The
high density of the contrast in
the collecting systems is
obscuring the sumucosal
granulomas; however,
irregularity along the medial
pelvic margin gives a clue to
the presence of the same (solid
arrowheads)

20. (A) Intravenous urogram revealing a “hiked up” renal pelvis (arrow). Tuberculosis cavity (white
arrowheads) communicating with the upper group of calyces. Black arrowheads represent medial
border of a compound upper calyx, (B) Intravenous urogram revealing fluffy cavities (white
arrowheads) communicating with a compound upper calyx (black arrowheads). Odd-shaped
pockets of contrast communicating with a lower calyx (and with each other) [circled area], represent
caseated necrotic cavities

21. (A) Intravenous urogram revealing a non-functioning (L) kidney and a small capacity urinary
bladder. The combination is suggestive of a
tuberculosis origin for the non-function, (B) Intravenous urogram revealing non-functioning (R)
kidney. (L) Renal pelvic and upper
infundibular scarring (white arrowheads), resulting in uneven caliectasis. A (L) lower ureteric
stricture (arrow) and small capacity bladder
(black arrowheads)

22. Pyelo-cavitatory
(arrowheads)
and
pyelo-lymphatic
reflux (arrows)
noted on
retrograde
pyelography

23. Intravenous urogram revealing right upper infundibular (arrow) and calyceal
strictures, with cortical scarring. Pyelosinus extravasation of
contrast in the (L) kidney (arrowheads) suggests the presence of fragile calyces

24. Delayed phase of intravenous urogram with a non-functional (L) kidney opacified retrogradely: Developing lobar
caseation in the U/3 of the (L) kidney (black arrowheads).
Note assimilation of the dilated calyces into the renal parenchyma.
Ragged hydrocalicosis(indicative of marked urothelial thickening) noted in the lower half of the (L) kidney (arrows).
Parenchymal demarcation is still clear adjacent to the same
(dotted line represents the non-visualized left renal outline).
(R) renal papillary necrosis is also seen (circled area) and so are calcified (L) paraspinal lymph nodes (white
arrowheads)

25. (A) Intravenous urogram revealing calcified (L) psoas abscess (black arrow), impinging
on the ureter and a calcified caseous renal mass
(arrowheads); more apparent on nephrotomography (B)

26.  Sonographic appearances are non-specific and variable, depending on
the stage of disease.
 early
› normal kidney or small focal cortical lesions with poorly defined border
› +/- calcification.
 progressive
› papillary destruction with echogenic masses near calyces
› distorted renal parenchyma
› irregular hypoechoic masses connecting to collecting system; no renal pelvic
dilatation
› mucosal thickening +/- ureteric and bladder involvement
› small, fibrotic thick-walled bladder
› echogenic foci or calcification (granulomas) in bladder wall near ureteric orifice
› localised or generalised pyonephrosis
 endstage
› small, shrunken kidney, "paper-thin" cortex and dense dystrophic calcification in
collecting system.
› may resemble chronic renal disease

27.  Ultrasound is less sensitive than CT in
detection of:
 calyceal, pelvic or ureteral abnormalities.
 isoechoic parenchymal masses.
 small calcifications.
 small cavities that communicate with
collecting system.

28. (A) USG revealing
tuberculosis
granulomas of varying
sizes (white arrows),
(B) USG revealing
larger granulomas–
the granulomas are
highlighted by the
vascular “cut-off”
(white arrows) noted
on this color flow
image

29. (A) High-resolution ultrasound images (acquired with a 7.5 MHz transducer) demonstrate a small
irregular caseous cavity (white arrow) in
the upper part of the left renal parenchyma, (B) high-resolution ultrasound images revealing a
tuberculous cavity with fine septae within, in
the lower part of the left kidney of another patient. Note marked urothelial thickening in this dilated
system, (C) USG image revealing irregular
sonolucent cavities, with a semisolid echo texture

30. USG image revealing an xanthogranulomatous pyelonephritis-like
appearance in an enlarged tuberculous kidney

31. (A) USG image revealing a
caseating tuberculous
granuloma, communicating with
a calyx via a narrow tract (white
arrows), (B) USG image
revealing a large thick walled
caseated tuberculous cavity
communicating with the upper
calyx (arrowheads). Small
granulomas are noted inferior to
this cavity (arrows)

32. (A) USG image revealing hyperechogenic areas of caseation interspersed with the echogenic sinus
echoes. (coronal scan), (B) Oblique USG scan reveals uneven caliectasis (white arrows) with a
hazy interface and urothelial thickening in the upper calyces. The lower calyceal region is replaced
by hyperechogenic caseous tissue, (C) Comparative USG image of regular (evenly dilated)
caliectasis with hyperechoic fungal balls (white arrows) in a HIV-positive patient (note the
hyperechogenic material is lying within clearly dilated calyces and are not replacing them as
happens in tuberculous caseation)

33. (A) Moderate-to-severe
urothelial thickening noted
throughout the visualized
urothelium. This is well
visualized on account of the
dilatation due to a tuberculous
ureteric stricture, (B) USG
image revealing uneven
caliectasis with ragged
urothelial thickening
(arrowheads). Note significant
debris in the lower calyces

34. USG image showing evolution of tuberculous lobar caseation. Different phases of
destruction are apparent. (Lower group calyces are completely merged with the
parenchyma, midgroup calyces about to merge, and upper ones almost merged).
Arrowheads demarcate the junction between residual parenchyma and the dilated
calyces

35. (A) USG image revealing caseation with a developing lobar pattern of calcification, in
almost all calyces, barring the lower group of calyces (white arrow) (B) USG image
revealing classic “lobar calcification”- pathognomonic of renal tuberculous (C) USG
image revealing a densely calcified kidney producing acoustic shadowing that obscures
underlying details. White arrows point to junctions between the renal lobes

36.  (A) USG image
revealing lobar
caseation (A) Grey
scale and, (B) Color
flow image
demonstrating
presence of renal
vasculature only
between the
caseated lobes

37. (A) USG image revealing left
tuberculous perinephric
collection due to a ruptured
upper polar tuberculous
abscess. (A) Grey scale
image, (B)
USG image revealing left
tuberculosis perinephric
collection due to a ruptured
upper polar tuberculous
abscess. Color flow image
revealing
lateral extent of the renal
parenchyma

38.  CT is the most sensitive modality for visualising renal
calcifications and CT IVP is more sensitive at identifying all
manifestations of renal tuberculosis .
 early
› papillary necrosis (single or multiple) resulting in uneven caliectasis
 progressive
› multifocal strictures can affect any part of the collecting system
› generalised or focal hydronephrosis
› mural thickening and enhancement
› poorly enhancing renal parenchyma, either due to direct involvement or
due to hydronephrosis
 endstage
› progressive hydronephrosis results in very thin parenchyma, mimicking
multiple thin walled cysts
› amorphous dystrophic calcification eventually involves the entire kidney
(known as putty kidney)

39. Renal
tuberculosis.
Contrast
enhanced
nephrographic
phase CT shows
dilated
calices and
thining of the
renal cortex with
thin calcifications.

40. CT revealing parenchymal granulomas (black arrows) in
the (L) kidney with uneven caliectasis and ureterectasis accompanied
by urothelial thickening (white arrow). Note the hypoperfused renal
parenchyma and complete loss of corticomedullary differentiation in
the (L) kidney

41. (A) Nephrographic and (B)
pyelographic phase
of CT: Showing a peripherally
enhancing granuloma (arrow) in
a
horseshoe kidney. Diffuse
inflammation mimicking a lobar
nephronia-like
appearance is also noted, with
perinephric extension (circled
area).
Note loss of corticomedullary
differentiation in (A) in the left
third of this
kidney

42. CT revealing caseous TB cavity (arrow) in the upper
pole of the (L) kidney: (A) axial and (B) coronal sections (MIP image).
Note non-functioning hydronephrotic (R) kidney, with a scarred renal
pelvis, in (B), which is a delayed scan

43. Axial CT revealing tiny granulomas (arrows) in both
kidneys, better appreciated on the (R). A left renal abscess with
perinephric extension. Note bilateral fascial thickening (arrowheads),
additional (B) axial and (C) coronal CT images revealing site of rupture into
the perinephric space (arrows). Drainage catheters are noted bilaterally

44. CT revealing Left TB renal
abscess (arrow) with
minimal perinephric spread
(arrowheads) in (A). The left
psoas muscle
is involved, better appreciated
in (B), Retroperitoneal fascial
thickening,
fat stranding, and small left
paraaortic lymph nodes are
also noted
with a loss of corticomedullary
differentiation of the affected
area in
the (L) kidney

45. CT revealing (A) focal renal cortical scarring (arrows)
and (B) focal cortical thinning (C) diffuse cortical scarring of the (L) renal
cortex. Renal pelvic scarring and resultant caliectasis are also noted

46. (A) Non-contrast CT image showing fine cortical calcification in the (L) kidney (white
arrow).
(B) The cavity (arrowheads) was communicating with the PCS. The urothelial thickening
(black arrow) is also well appreciated.
(B and C) non-contrast CT image showing punctate calcification [arrows in (B) and soft
(caseous) parenchymal calcification arrowheads in (C)].
(D and E) axial CT revealing the lobar pattern of calcification (arrowheads)

47. CT revealing multiplicity of
findings in urinary TB-uneven
caliectasis with no obvious
pelvic dilatation, parenchymal
scarring
(black arrow), cavity
communicating with PCS
(white arrow), urothelial
thickening and multiple
ureteral strictures (black
arrowheads)

48. (A) Axial and (B) coronal CT images revealing lobar
caseation of the (L) kidney. Note assimilation of the calyces into the renal
parenchyma. The calyces in the (R) sided hydronephrosis communicate
with each other and are clearly demarcated from the renal parenchyma.
Note the stricture of distal ureter with resultant proximal dilatation

50. Fat-saturated T2W FSE sequence MRI image showing
multiple small hypointense granulomas (thin white arrows) in the (R)
kidney. The (L) kidney shows caliectasis with heterogeneous intermediate
signal within on T2W images, due to caseous internal debris (thick arrow)

51. Fat-saturated T2W FSE sequence MRI image showing
small, slightly hyperintense, caseating granulomas (curved arrows),
and a tiny hypointense non-caseating granuloma (arrow)

52. (A) axial fat-saturated T1W FSE, (B) Coronal fat-saturated T2W FSE sequence and (C) post-contrast axial T1 fat-
saturated MRI images of the patient reveals multilocular cystic appearance in a case of tuberculous
pyonephrosis on right side.
There is significant global thinning of the renal parenchyma. The cystic lesions are predominantly hyperintense,
but reveal multiple scattered areas of intermediate signal within, along with few septae (black arrow).
The left upper pole renal lesion appears slightly hyperintense on T2-weighted images suggestive of a focal area
of caseous necrosis (white arrow)

53. (A) axial and (B) coronal fat-saturated T2W FSE
sequence and (C) post-contrast axial T1 fat-saturated MRI imagesshowing
a TB cavity (arrowheads) communicating with dilated calyces.
Note small peripheral non-enhancing hypointense lesion, suggestive of a
granuloma (white arrow). An enlarged pyramid is also noted (black arrow)

54. Fat-saturated
T2W coronal
MRI image of TB
pyonephrosis
revealing a
scarred renal
pelvis and
marked dilatation
of the collecting
system with
severe
parenchymal
loss

55.  Renal angiography shows no specific vascular
changes in renal TB.
 The vessels appear normal in the early case,
 while in the more advanced case, there may be
zones of irregularity (especially of the interlobar
and arcuate arteries) and even complete
occlusion.
 In instances of TB pyonephrosis, angiography
reveals the appearance of hydronephrosis.

56.  Angiography is of greater help in determining
how much viable renal tissue remains and in
the planning of partial nephrectomy than it is
in the specific diagnosis of TB.

57.  Multi-drug treatment is essential, however
despite treatment, stricturing can progress.
 The role of nephrectomy is controversial and
depends on the degree of renal impairment,
bilateral vs unilateral disease and the status
of the lower urinary tract.
 Nephrectomy, partial nephrectomy or
cavernostomy can be performed both open
and endoscopically

58.  General imaging differential considerations
include:
 papillary necrosis
 medullary sponge kidney
 TCC (transitional cell carcinoma) of renal tract
 SCC (squamous cell carcinoma) of renal tract
 xanthogranulomatous pyelonephritis (XGP)


59. Thank you