Several factors associated with ESA responsiveness have been reported in HD patients. However, there is little information in PD patients. We investigated the factors which affect ESA doses in PD patients. Methods: Among 53 patients undergoing PD in our hospital, we analyzed the patients who were selleck kinase inhibitor changed to C.E.R.A. from current ESA, and followed-up for 1 year. Target hemoglobin levels were 11–13 g/dl according to the Japanese Society for Dialysis Therapy’s guidelines for renal anemia. We analyzed a univariate analysis for factors that might influence on Hb concentration and on the dose of CERA at switching time and one year later. Results: The mean age was 57.9 ± 12.2

years, and the mean duration of PD was 46.8 ± 22.1 months. Mean weekly Kt/V was 1.89 and mean

residual urine volume was 1153 ml/day. Rucaparib Hemoglobin levels remained unchanged from 11.4 g/dl at the start of therapy to 11.5 g/dl 12 months thereafter. Univariate analysis indicated that factors associated with Hb levels when starting CERA were CRP > 0.3 mg/dl, Alb 0.5 and serum β2MG < 30, lower doses of CERA is required (P = 0.004, P = 0.007, respectively). Conclusion: Patients whose residual renal function preserved were prone to have lower ESA requirements. To maintain residual renal function is important for management of renal anemia in PD patients. SHIN HYUN-SOO, RYU EUN-SUN, CHOI Cell press HAK-SUN, RYU DONG-RYEOL, CHOI KYU-BOK, KANG DUK-HEE Division of Nephrology, Ewha Womans University School of Medicine, Seoul, Korea Introduction

and Aims: Phenotype transition of peritoneum has been regarded as an early mechanism of peritoneal fibrosis. Metformin, 5′-adenosine monophosphate (AMP)-activated protein kinase activator, is a drug widely used to treat type 2 diabetes and also a key player in the regulation of energy hemostasis. Metformin has recently received a new attention due to its therapeutic effect in oncology by inhibiting epithelial-to-mesenchymal transition (EMT). We investigated the effect of metformin on EMT of HPMC and cellular mechanism for this beneficial effect of metformin on peritoneal EMT and fibrosis. Methods: EMT was evaluated by morphological changes of HPMCs and the expressions of epithelial cell marker, E-cadherin and mesenchymal cell marker, α-smooth muscle actin (α-SMA) after stimulation of TGF-β1 (1 ng/ml) with or without metformin (1 mM) by real time PCR, western blotting and immunocytochemistry. Intracellular reactive oxygen species (ROS) were analyzed by DCF-DA, NADPH activity, NADPH oxidase mRNA expressions, and MitoSoxR staining. Activation of Smad2/3, Erk1/2, p38 MAPK, nuclear translocation of β-catenin and snail expression were assessed by western blotting and immunocytochemistry.