5%, p <0.05), better maintenance of MAP (93.8% vs. 72.5%, p=0.02) with cessation of vasopressor requirement (50% versus 25% p=0.03) at 48 hours, improved urine output at 24 hours (59% versus 36%, p=0.05) and no variceal

bleed (0% versus 15.45%, p=0.03) without significantly increased adverse effects (40.6% vs. 22.5%, p=0.12). Terlipressin use showed delayed resolution of Acute Kidney Injury on fifth day (59.4% vs. 16.75, p=0.08) with improved lactate clearance, Central Venus Oxygen saturation and CO2 gradient in Venous – arterial blood gases (p=NS). An early survival advantage was seen with the use of terlipressin (93.5% vs. 75%, p=0.02) in the first 48 hours, but not at 28 days. Conclusion: Terlip-ressin as a vasopressor is non-inferior to noradrenaline with greater hemodynamic stability, early survival benefit, improved urine output, reduced variceal bleed Selleckchem SCH772984 and decreased incidence of nosocomial SBP with nonfatal and reversible adverse effects. Its use is recommended in decompensated

cirrhotics presenting with septic shock. Disclosures: The following people have nothing to disclose: Ashok K. Choudhury, Chitranshu Vashishtha, Deepak Saini, Sachin Kumar, Shiv K. Sarin Background and Aims: HRS-1 is a reversible form of acute kidney injury in cirrhotics with ascites. The aim of REVERSE was to define the efficacy and safety of terlipressin plus albumin versus selleck albumin alone for the treatment of HRS-1. Methods: HRS-1 was defined as rapidly deteriorating renal function (SCr ≥2.5 mg/ dL and actual or projected doubling of SCr within 2 weeks) without improvement in renal function (<20% decrease in SCr and SCr ≥2.5 mg/dL) 48 hours after both diuretic withdrawal and albumin-fluid challenge in adult cirrhotics with ascites. Subjects were randomized to terlipressin (1 mg IV every 6 hours) or placebo, plus

albumin in both groups. Treatment was continued to Day 14 unless the following occurred: confirmed HRS reversal (CHRSR), renal replacement therapy (RRT), transplantation or SCr at or above baseline at Day 4. CHRSR was defined as 2 SCr values ≤1.5 mg/dL, at least 48 hours apart, on treatment, selleck chemical without RRT or liver transplant; HRS reversal was a decrease in SCr to ≤1.5 mg/dL. Results: 196 subjects were enrolled; 97 were randomized to terlipressin, 99 to placebo. Demographic and baseline clinical characteristics were similar between treatment groups. CHRSR, the primary endpoint, was observed in 19/97 patients (19.6%) in the terlipressin group vs. 13/99 patients (13.1%) in the placebo group (p = 0.2214); a higher percentage of patients in the terlipres-sin group achieved HRS reversal (23/97; 23.7%) compared with placebo (15/99; 15.2%) (p=0.1296). The change from baseline to end of treatment in SCr was significantly greater for terlipressin vs. placebo (terlipressin -1.2, placebo -0.6, ter-lipressin vs. placebo -0.6 mg/dL, p = 0.0003); there was significant correlation between improvement of SCr and survival (r2 = 0.7274, p=0.0035).