Although PVT carries independent prognostic value for a poorer outcome, it is not a direct cause for aggravation. These data point to PVT and aggravation as discrete consequences of a common determinant for progression of cirrhosis, e. g. hepatic or intestinal microcirculatory dysfunction. Disclosures: Dominique Valla – Board Membership: Sequana Medical; Independent Contractor: IRIS; Speaking and Teaching: Mayoly
Spindler, MSD, Janssen Pharmaceuticals The following people have nothing to disclose: Filipe G. Nery, Cendrine Chaffaut, Bertrand Condat, Emmanuelle de Raucourt, Larbi Boudaoud, Pierre-Emmanuel Rautou, Aurelie Plessier, Dominique Roulot, Jean Claude Trinchet, Sylvie Chevret Background EX 527 purchase and Aims: The current definitions
for AKI and Hepatorenal syndrome (HRS) have been derived from patients with cirrhosis (CLD). There is paucity of data on AKI in patients with ACLF. We investigated the prevalence, spectrum, natural history and outcome of AKI in patients with ACLF [Asian Pacific Association for Study of Liver, (APASL), definition] and compared it with a cohort of hospitalized patients with cirrhosis. We also compared outcome and response to terlipressin in HRS (International Ascites Club) in both the groups. Methods: AKI was defined according to Acute Kidney Injury Network (AKIN )criteria. Serial creatinine until improvement or upto day 30 was recorded for all patients. Results: Patients with AcLF (n=534) were predominantly Gefitinib ic50 males (p<0.0001), younger (p<0.0001) with higher serum bilirubin (p<0.0001), INR (p<0.0001), hepatic encephalopathy (p<0.0001), GI bleed (p<0.0001) and mortality (p<0.0001) as compared to CLD (n=2083). AKI
at baseline was significantly more common in patients with ACLF (50.5% vs. 32.3%; p<0.0001) and associated with increased risk of mortality (59.9% vs. 41.3%; p<0.0001) as compared to CLD. A significant difference was also observed in the spectrum of AKI (p<0.0001) with sepsis related AKI as commonest cause in ACLF (160; 58.8%) and prerenal (289; 43%) in CLD. Presence of ACLF (vs CLD) was associated with a six-fold increased risk of AKI (p<0.0001, OR 95% CI 4.9-8.3) on multivariate analysis. There was no significant difference seen in the AKIN stage at baseline (Stage 1 : 61% vs 69%; Stage 2: 29.5% vs 23.5%; Stage 3: 9.9% vs 8.5%), decrease in serum creatinine at selleck screening library 48 hours (67.3% vs 65.3%) and in the overall progression of AKI (48.5%vs 45.1%), however, requirement of renal replacement therapy (RRT) and progression to AKIN stage 3 (23.5% vs 12.6%) was significantly more common in ACLF (p<0.0001). Presence of HRS (28.7% vs 29.2%) and response to terlipressin (44.1% vs 44.3%) was not significantly different in both the groups, however HRS in ACLF was characterized by an increased mortality (67.9% vs 45.9%; p=0.001) and progression to acute tubular necrosis (ATN) with higher need of RRT (53.8%vs 20.4%; p<0.