Recent advances in our understanding of hepatorenal syndrome

Abstract

Hepatorenal syndrome (HRS) is a serious complication of advanced cirrhosis with ascites. HRS develops as a result of abnormal haemodynamics, leading to splanchnic and systemic vasodilatation, but renal vasoconstriction. Increased bacterial translocation, various cytokines and mesenteric angiogenesis also contribute to splanchnic vasodilatation, and altered renal autoregulation is involved in the renal vasoconstriction. Type 1 HRS is usually initiated by a precipitating event associated with an exaggerated systemic inflammatory response that perturbs haemodynamics, resulting in multiorgan failure. An inadequate cardiac output with systolic incompetence increases the risk of renal failure. Vasoconstrictors are the main treatment in patients with type 1 HRS; terlipressin is the superior agent. Norepinephrine is similar to terlipressin in efficacy and can be used as an alternative. Transjugular intrahepatic portosystemic stent shunt might be applicable in a small number of patients with type 1 HRS and in most patients with type 2 HRS. Liver transplantation is the definitive treatment for HRS, and should be performed after reversal of HRS. In nonresponders to vasoconstrictor therapy, much controversy still exists as to whether to do simultaneous or sequential liver and kidney transplant. In general, patients who have had >8-12 weeks of pretransplant dialysis should be considered for combined liver-kidney transplantation.