Acute kidney injury and hepatorenal syndrome in decompensated liver cirrhosis

Abstract

For patients with decompensated cirrhosis, renal impairment is commonly observed, and occurs in approximately 20% of hospitalized patients. Hepatorenal syndrome (HRS) occurs typically in the setting of portal hypertension and ascites. This is presumably due to systemic and splanchnic arterial vasodilatation with renal vasoconstriction, leading to impairment in renal perfusion. Specific therapies directed at improving renal perfusion are effective in the treatment of HRS. However, acute kidney injury (AKI) is commonly observed in patients with decompensated cirrhosis, and not all are related to HRS, or fulfill the stringent diagnostic criteria for HRS. The proposed definition for AKI is an increase in serum creatinine by 0.3 mg/dl within 48 hours or an increase by 50% from baseline within 3 months. Both may be precipitated by an acute event, most commonly a preceding infection. It has long been known that the development of HRS was associated with poor short and medium term survival. More recently, AKI has been shown also to be predictive of poorer outcome including higher complication rates, longer hospital stay, and higher short–term mortality. The effects of non–selective beta–blockers on renal function remain controversial, but caution should be exercised for patients with ascites and hypotension. It is likely that the definition of renal dysfunction observed in decompensated cirrhosis will continue to evolve, with AKI and HRS forming a spectrum of renal impairment in cirrhotic patients. Early identification of renal dysfunction will allow for treatment to be started in a timely manner, and may be able to prevent the development of HRS.