Abstract
Background: Acute kidney injury is present in a third of hospitalized patients with cirrhosis. AKI in cirrhosis can be functional (Pre renal azotemia and Hepatorenal syndrome) or structural (Acute tubular necrosis). Distinguishing the precise etiology of AKI in cirrhosis remains a clinical challenge. Fractional excretion of sodium as a marker of functional AKI has several limitations.
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