The hepatorenal syndrome (HRS) is related to vasoconstriction of the renal cortex induced by systemic hypovolemia that follows splanchnic vasodilatation as the primary event in the cascade of hemodynamic changes associated with portal hypertension. We evaluated the effects of octreotide, a splanchnic vasoconstrictor, on HRS in cirrhotic patients. We compared the effects of octreotide infusion (50 g/h) to placebo using a randomized, doubleblind, cross-over design over 2, 4-day periods. Nineteen patients were included, and 14 patients could complete the 2 phases of the study (group 1: placebo first; n ؍ 8 and group 2: octreotide first; n ؍ 6) The end point of the study was to evaluate improvement in renal function as defined by a 20% decrease in serum creatinine value after a 4-day treatment as compared with baseline. In all the patients, a normal central venous pressure was maintained by daily intravenous administration of 2 units of albumin. The 2 groups were similar with regard to demographic data and liver and kidney function parameters at baseline. Improvement in renal function was observed in 2 patients after the placebo and 1 patient after octreotide infusion in group 1 and in 2 patients after octreotide infusion and 1 patient after placebo in group 2 (P ؍ not significant). In addition, treatment with octreotide infusion did not result in significant changes in creatinine clearance, daily urinary sodium, plasma renin activity, plasma aldosterone and glucagon levels, or renal and mesenteric artery resistance indices as measured by Doppler ultrasonography. In conclusion, the present study demonstrates that, under our experimental conditions, octreotide infusion combined with albumin is not effective for the treatment of HRS in cirrhotic patients. (HEPATOLOGY 2003;38:238-243.) T he hepatorenal syndrome (HRS) is a functional renal disorder associated with severe acute or chronic liver failure. It is always potentially reversible because no anatomic damage can be demonstrated in the kidney. This syndrome carries a very bad prognosis because it is always the consequence of severe liver insufficiency, the only definitive treatment being liver transplantation. 1 The pathophysiology of renal failure is thought to be mediated primarily by splanchnic vasodilatation leading to systemic hypovolemia; a cascade of vasoactive mechanisms is then initiated including compensatory activation of vasoconstrictor catecholamines, renin, aldosterone, antidiuretic hormone, and endothelin; a marked vasoconstriction of the renal cortex ensues, glomerular filtration decreases, and the kidney function deteriorates. 2 Over recent years, several attempts have been made to correct the cortical renal vasoconstriction by using splanchnic vasoconstrictors, in the hope of reversing splanchnic vasodilatation, which is thought to be the primary pathogenetic event. The efficacy of ornipressin, 3-5 terlipressin, 6-10 and octreotide alone 11 or combined with midodrine 12 has been tested in small uncontrolled pilot trials. Terlipressin appe...