Hepatorenal syndrome (HRS) is characterized by functional renal impairment in patients with end-stage liver cirrhosis and no parenchymal kidney disease. It is due to splanchnic vasodilation, which results in renal vasoconstriction with consequent reduction in renal plasma flow and glomerular filtration rate.1 In the United States, treatment is with a combination of octreotide, midodrine, and human albumin to increase the effective blood volume and subsequently improve renal function.2 While octreotide, a long-acting somatostatin analog, is used to induce splanchnic vasoconstriction in this setting, it also affects the secretion of insulin and glucagon.