Neutrophil-gelatinase associated lipocalin (NGAL) is an iron-transporting Deforolimus price protein with increased renal excretion in nephrotoxic

or ischemic kidney injury. We aimed to test the hypothesis that urinary NGAL measurement is useful to monitor acute kidney injury in cholemic nephropathy. Methods: Chow-fed (controls) or norUDCA (0.125% w/w)-treated CL57/BL6 mice were subjected to CBDL for 8 weeks. Urinary NGAL levels were determined at time of harvesting using a commercially available ELISA kit (Lipocalin-2/NGAL DuoSet Mouse, R&D Systems, DY1857). In brief, samples were incubated with detection antibody, labeled with streptavidin-HRP and subsequently measured at 450 nm. Results: Chow-fed CBDL mice exhibited significantly elevated

urinary NGAL levels (29.6 ± 4.2 ng/ ml) compared to norUDCA-treated CBDL mice (9.4 ± 1.8 ng/ ml, p<0.05). NorUDCA treatment significantly ameliorated the degree of DNA Damage inhibitor nephritis and kidney fibrosis and consequently to a significantly reduced renal hydroxyproline content (466 ± 107 μg/g vs. 797 ± 160 μg/g in controls, p<0.05). Conclusions: Urinary NGAL measurement represents a suitable readout for monitoring the degree of cholemic nephropathy in CBDL mice and reflects the therapeutic effects of norUDCA. Future studies should determine urinary NGAL levels in patients with cholemic nephropathy. Disclosures: The Medical University of Graz has filed a patent for the use of norUDCA in the treatment of liver diseases, and P.F. and M.T. are listed as co-inventors (publication number WO2006119803) and P.F. received a research grant and norUDCA from Dr. Falk Pharma GmbH for this project. Disclosures: Michael Trauner - Advisory Committees or Review Panels: MSD, Janssen, Gilead, Abbvie; Consulting: Phenex; Grant/Research Support: Intercept, Falk Pharma, Albireo; Patent Held/Filed: Med Uni Graz (norUDCA);

Speaking and Teaching: Falk Foundation, Roche, Gilead Peter Fickert – Consulting: Falk Foundation, Falk Foundation, most Falk Foundation, Falk Foundation; Speaking and Teaching: Roche Austria, Gilead Austria, MSD Austria, MERCK Austria, Roche Austria, Gilead Austria, MSD Austria, MERCK Austria, Roche Austria, Gilead Austria, MSD Austria, MERCK Austria, Roche Austria, Gilead Austria, MSD Austria, MERCK Austria The following people have nothing to disclose: Elisabeth Krones, Dietmar Glaenzer, Franziska Durchschein, Alexander Kirsch, Kathrin Eller, Alexander R. Rosenkranz Patients with cirrhosis develop hyperdynamic circulation with an increase in cardiac output (CO) and a decrease in systemic vascular resistance (SVR). Patients with hyperdynamic circulation can develop circulatory dysfunction(CD) when this compensatory mechanism is insufficient. Although this takes place theoretically in decompensated patients, namely in patients with ascites, its prevalence has never been specifically analysed.