RENAL TUBERCULOSIS

Dr Ashish Kumar GuptaPg Radiodiagnosis

Slims

Renal tuberculosis 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.

Clinical presentation Clinical features are often non specific

and include: Dysuria; Pyuria; Back , flank pain or abdominal pain Microscopic or macroscopic haematuria Constitutional symptoms

Pathology 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. 

Tuberculosis Of Urinary Tract

pathological changes of renal tuberculosis

pathological changes of renal tuberculosis

Radiographic features

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

Radiographic features 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

Plain film

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)

Calcifications of tuberculosis

(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 kidneyby inflammatory debris

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

Fluoroscopy: IVP 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

Tuberculosis Retrograde pyelogram

Collimated image from intravenous urography demonstratesmultiple 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 well.

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

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

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)

(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)

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)

(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

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

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

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

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)

(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)

Ultrasound 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

Ultrasound

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.

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

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

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

(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)

(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)

(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

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

(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

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

(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 revealinglateral extent of the renal parenchyma

CT 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)

ctRenal tuberculosis. Contrast enhanced nephrographic phase CT shows dilatedcalices and thining of the renal cortex with thin calcifications.

CT revealing parenchymal granulomas (black arrows) inthe (L) kidney with uneven caliectasis and ureterectasis accompaniedby urothelial thickening (white arrow). Note the hypoperfused renalparenchyma and complete loss of corticomedullary differentiation inthe (L) kidney

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

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

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

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

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

(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)

CT revealing multiplicity of findings in urinary TB-unevencaliectasis with no obvious pelvic dilatation, parenchymal scarring(black arrow), cavity communicating with PCS (white arrow), urothelialthickening and multiple ureteral strictures (black arrowheads)

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

MRI

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

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

(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)

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

Fat-saturated T2W coronal MRI image of TB pyonephrosisrevealing a scarred renal pelvis and marked dilatation of the collectingsystem with severe parenchymal loss

Angiography

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.

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.

Treatment and prognosis

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 

Differential diagnosis

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)

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