Hepatorenal syndrome (HRS) is a type of renal failure that occurs in patients with advanced cirrhosis. It is a result of splanchnic arterial vasodilation, renal vasoconstriction, reduced effective arterial volume, and potentially reduced cardiac output. Often, HRS is a fatal complication, and the only definitive treatment currently available is liver or liver-kidney transplantation. A number of other treatment modalities have been tested for the management of HRS, but most evidence is derived from small noncontrolled studies. The primary role of these treatment options is to provide a bridge to liver transplantation. Treatment may also provide acute reversal of renal failure and some symptomatic relief, but relapse is a common occurrence. The best therapeutic options appear to be those that reverse portal hypertension, splanchnic vasodilation, and/or renal vasoconstriction. Vasopressin analogs, particularly terlipressin, have emerged as the preferred pharmacologic therapies for management of HRS. Albumin is an appropriate adjunctive therapy to terlipressin and can be used to prevent HRS in patients with spontaneous bacterial peritonitis. Transjugular intrahepatic portosystemic shunt may provide a surgical option for qualified patients with HRS. Octreotide is ineffective as monotherapy but may be used as adjunctive therapy to other vasoactive agents. Dopamine agonists, endothelin antagonists, natriuretic peptides, and nitric oxide synthase inhibitors have not been effective for reversing HRS. Artificial hepatic support therapies have demonstrated the ability to improve laboratory abnormalities in patients with HRS, but their effect on clinical outcomes has not been determined. The role of renal replacement therapies or the newer artificial hepatic support therapies need further evaluation before they can be routinely recommended.