Hepatorenal Syndrome: New Understanding and Management

Abstract

Hepatorenal syndrome (HRS) is a major complication of decompensated liver cirrhosis, with associated high mortality without liver transplantation. In recent years, the paradigm of HRS has shifted from that of a solely functional renal impairment secondary to hypoperfusion, to a more direct role involving increases in the levels of pro-inflammatory cytokines. This new theory implicates not only a circulatory component, but also the involvement of an inflammatory component in the pathophysiology of HRS. Acute kidney injury (AKI) is commonly seen in hospitalized cirrhotic patients, and HRS-AKI represents only one of many types of AKI, including pre-renal AKI, intrinsic AKI, and postrenal AKI. The diagnosis of HRS requires the exclusion of these other causes of AKI, which is often difficult in the absence of reliable renal biomarkers. The use of vasoconstrictive drugs together with albumin remains the cornerstone of HRS management to improve renal perfusion and to reverse the splanchnic vasodilatation. The use of renal replacement therapy should be individualized according to the disease severity and whether it fulfills the indication for dialysis treatment. Liver transplantation continues to be the definitive therapeutic option for patients with HRS.