Abstract
Background and Aim: Acute renal failure (AKI) is a common complication of decompensated cirrhosis and confers a poor prognosis. AKI in these patients may result from functional decrease in renal function as in prerenal azotaemia (PRA) and Hepato-renal syndrome (HRS) or due to structural renal abnormalities as in acute tubular necrosis (ATN). These phenotypes of AKI have therapeutic and prognostic implications. However, in clinical practice, approaches to determine the cause of AKI in these patients are suboptimal.
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