The exact pathologic mechanism for RCN is unclear, however the onset of small vessel pathology is likely an important aspect in the cause of this condition. In general the renal cortex is under greater oxygen tension and more prone to ischemic injury, especially at the level of the proximal collecting tubule, leading to its preferential damage in a sudden drop in perfusion. Rapidly corrected acute renal ischemia leads to acute tubular necrosis, from which complete recovery is possible, while more prolonged ischemia may lead to RCN. Pathologically, the cortex of the kidney is grossly atrophied with relative preservation of the gross structure of the medulla. The damage is usually bilateral owing to its underlying systemic causes, and is most frequently associated with pregnancy (>50% of cases). It accounts for 2% of all cases of acute kidney failure in adults and more than 20% of cases of acute kidney failure during late pregnancy.
Renal cortical necrosis
Renal papillary necrosis
Acute tubular necrosis
Glomerulonephrosis
Pyonephrosis
Renal vein thrombosis
Ureteric stricture
Shunt nephritis