Putty kidney

4,207 views 25 slides Feb 03, 2018
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About This Presentation

End stage of Renal Tuberculosis


Slide Content

Putty kidney Dr. Mahesh C haudhary Resident phase - B Radiology & imaging, BSMMU

Introduction A putty kidney  refers to a pattern of renal calcification associated with renal tuberculosis conventionally described on plain radiography. Calcification is usually homogeneous and ground glass-like, representing calcified caseous tissue Premkumar et al. Labelled calcification 'putty-like' if any faint area of uniform calcification was more than 1 cm in diameter  Lobar calcification represents an end-stage appearance, associated with autonephrectomy .

gENITOurinary tuberculosis The genitourinary tract is a primary target of hematogenous infections and is the most common site of extra-pulmonary TB Genitourinary tuberculosis (GUTB), a term coined by W ildbolz in 1937 A worldwide disease, but shows a more destructive behavior in developing countries The kidney is the most common site of GUTB Increased incidence of extra-pulmonary TB has been noted in AIDS

Patient Population GUTB usually affects adults between the second and fourth decades of life There is often a long latent period (5-40 years) between the original pulmonary infection and the appearance of clinical renal disease, which is probably why renal involvement is rare before the age of 20 years

Symptoms Frequent voiding; dysuria; pyuria Back, flank or abdominal pain Microscopic or macroscopic hematuria Hematuria and culture-negative pyuria may be seen at urine analysis Urine analysis of sediment from a 24-hour specimen for acid-fast bacilli (AFB) is positive in 80-90% of cases of TB

Renal tuberculosis 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

Pathology Renal infection results from hematogenous spread at the time of primary infection, with multiple micro-abscesses developing at the site of peri -glomerular capillary seeding 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

Radiographic features Both the renal parenchyma and the upper collecting system (calyces and renal pelvis) can be involved 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

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)  End-stage Progressive hydronephrosis and parenchymal thinning Dystrophic calcification

Plain radiograph Plain film findings focus on calcification, which is seen in ~35% (range 25-45%), at various stages of disease: Triangular in papillary necrosis Focal or amorphous:  putty kidney  (end stage)

IVU Traditional plain film IVU is quite sensitive to renal tuberculosis. Features include: Parenchymal scars 50% Moth eaten calyces : early finding         Irregular caliectasis           Phantom calyx Hydronephrosis

Lower urinary tract signs Kerr kink   Sawtooth ureter Pipe-stem ureter Beaded or corkscrew ureter Thimble bladder

Ultrasound Sonographic appearances are nonspecific and variable, depending on the stage of disease.  Early Normal kidney or small focal cortical lesions with poorly defined border  Calcification +/- End-stage Small, shrunken kidney, "paper-thin" cortex and dense dystrophic calcification in collecting system May resemble chronic renal disease

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 localized or generalized pyonephrosis

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

CT CT is the most sensitive modality for visualizing 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 E nd-stage Progressive hydronephrosis results in very thin parenchyma, mimicking multiple thin walled cysts Amorphous dystrophic calcification eventually involves the entire kidney (known as putty kidney)

Progressive Multifocal strictures can affect any part of the collecting system Generalised or focal hydronephrosis Mural thickening and enhancement Poorly enhancing renal parenchyma, due to direct involvement or due to hydronephrosis

Treatment and prognosis Multi-drug treatment is essential, however despite treatment, structuring can progress The role of nephrectomy is controversial Nephrectomy, partial nephrectomy can be performed both open and endoscopically

Differential diagnosis Xanthogranulomatous pyelonephritis Rare form of chronic pyelonephritis and represents a chronic granulomatous disease resulting in a non-functioning kidney Female predilection (F:M 2:1) presumably relating to an increased incidence of urinary tract infections and thus struvite (staghorn) calculi. Nephrocalcinosis previous known as Anderson- Carr kidney or Albright's calcinosis, refers to the deposition of calcium salts in the parenchyma of the kidney Types: medullary nephrocalcinosis : 95% cortical nephrocalcinosis : 5 % combined cortical and medullary nephrocalcinosis Medullary sponge kidney Medullary sponge kidney is a sporadic condition where the medullary and papillary portions of the collecting ducts are dysplastic, and dilated and in most cases develop medullary nephrocalcinosis .

Xanthogranulomatous pyelonephritis A chronic granulomatous process The kidney is eventually replaced by a mass of reactive tissue, surrounding the usually present (90%) inciting staghorn calculus with associated hydronephrosis of a greater or lesser degree. Foamy (lipid-laden) macrophages predominate Fragmentation and enlargement of the the renal outline may be seen. A calculus is seen Medullary nephrocalcinosis D eposition of calcium salts in the medulla of the kidney. Due to the concentrating effects of the loops of Henle, and the biochemical milieu of the medulla, compared to the cortex, it is 20 times more common than cortical nephrocalcinosis Causes: hyperparathyroidism, medullary sponge kidney, renal tubular acidosis, hypervitaminosis D, milk-alkali syndrome, sarcoidosis . Hypercalciuric states Cushing syndrome multiple myeloma Bartter syndrome metastasis to bone Medullary sponge kidney It represents a developmental defect affecting the formation of collecting tubules and results in cystic dilatation of medullary and papillary portions of collecting ducts. Clusters of pyramidal medullary calcification are characteristic. Delayed post contrast CT may demonstrate a "paint brush" appearance to the renal medullary regions

XGPN Ultrasound examination demonstrates an enlarged and distorted renal outline, with loss of the normal renal architecture and (usually) a centrally-located shadowing calculus CT findings are most helpful in reaching the correct diagnosis. The normal renal outline is lost and enlarged with a paradoxical contracted renal pelvis. The calyces in contrast, are dilated giving a multiloculated appearance (paw print of a bear) Cortical nC Causes: renal cortical necrosis chronic glomerulonephritis Alport syndrome chronic pyelonephritis hyperoxaluria oxalosis vesicoureteral reflux (VUR) nephrotoxic drugs, e.g. Amphotericin B autosomal recessive polycystic kidney disease (ARPKD) Msk On IVP, pyelogram may give a characteristic bouquet of flowers appearance Ultrasound of the kidneys of patients with medullary sponge kidneys typically demonstrates echogenic medullary pyramids.

XGP Medullary NC Medullary sponge Kidney

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