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Congenital Anomalies

  1. MCDK
    1. In MCDK there is no normal overall structural pattern to kidney with loss of lobular organization although small islands of renal tissue are seen microscopically.
    2. MCDK is nonfunctioning and characterized by an atretic ureter without increased incidence of VUR.
    3. MCDK is usually unilateral and if bilateral, it is incompatible with life.
    4. On US, seen as a small single cyst to large mass containing multiple cysts with largest situated peripherally. Q
  1. Medullary cystic disease and Juvenile nephronopthisis
    1. Theses are two different terms for conditions, which differ in inheritance but have similar renal morphology and are radiologically indistinguishable. Both present with slowly progressive renal failure. MCD is autosomal dominant disease and presents up to 4th decade.
    2. USG reveal two normal sized kidneys with globally hyper-reflective appearance.   Cysts are not a feature until late in disease and are then typically corticomedullary.
    3. IVU is of little help in diagnosis if it is suspected on US. The 99mTc-DMSA scan may even fail to show the kidney. Ultimate diagnosis can only be made by rectal biopsy.
  2. Medullary sponge kidney:
    1. ’Bunch of flowers’ appearance i.e. thick dense streaks of contrast material radiating from pyramids peripherally “papillary blush” is normal people.Q
  3. Horseshoe kidneys: IVU appearance is characteristic:
    1. Kidneys are low lying with their upper poles directing superolaterally
    2. Lower pole calyces on both sides being directed inferomedially towards the midline
    3. PCS points anteriorly and rarely all or most of the calyces are reversed
    4. Q ‘Flower vase’ ureter deformity.
  1. ADPKD

  1. It is a bilateral renal cystic disorder which becomes manifest frequently after the 3rd decade of life.
  2. Gene is located on chromosome number 16 (in 90% cases) and 4.Q
  3. In ADPKD, there may be associated cysts in the liver (50% of cases), pancreas, spleen, lungs and testis. Other associations are berry aneurysms (which may cause SAH and severe headache), coarctation of aorta, valvular heart disease and colonic polyps.Q
  4. Congenital hepatic and periportal fibrosis is associated with ARPKD.Q
  5. IVU typically shows classical stretched appearance of calyces with some times spider leg appearance.
  6. USG typically reveals multiple bilateral (often asymetrical) non-communicating cysts of varying sizes, generally scattered throughout the cortex and medulla with normal intervening parenchyma and bilateral enlarged kidneys.
Extra Edge

Xanthogranulomatous Pyelonephritis (XGP): CT findings in XGP include loss of CM differentiation with calculi and low attenuation fatty masses replacing the renal parenchyma with some cystic/necrotic foci and perirenal fat stranding. Q

  • Renovascular hypertension
  1. It accounts for 1-4% of patients with hypertension.
  2. QAtherosclerotic disease is the most common cause of RAS, especially in elderly.
  3. Majority of patients are > 50 year old (M>F) and common at ostium or within proximal 2cm of renal artery, and bilateral in 1/3rd cases.
  4. QFibromuscular dysplasia (medial fibroplasias, medial or fibromuscular hyperplasia, intimal hyperplasia, perimedial fibroplasias) is the most common cause of Renovascular hypertension in children and young adults and bilateral in 2/3rd cases.
  5. Other causes of RAS are arterial dissection, aneurysms, thromboembolism, Buerger’s disease, Takayasu’s arteritis, neurofibromatosis, post-radiation and pheochromocytoma.
  6. Q “String of beads” appearance of FMD is classically seen on angiography.
  7. QRenal captopril radionuclide scan is a very sensitive mean of investigation.
  8. QHowever, investigation of choice is MRA.
  9. QACE inhibitors are contraindicated in bilateral RAS.
  10. Q Angiography is the gold standard and definitive means to diagnose RAS, except for the risk of contrast reaction.
Extra Edge
A stenosis is generally considered significant if the luminal diameter is reduced by 50% and the systolic pressure gradient is in excess of 10 mmHg across the lesion. 
A vessel lumen that is diminished by 50% will have a corresponding 75% reduction in a cross-sectional area, which will likely reduce flow to a clinically significant level. 

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