We evaluated daily doses and trough levels of Tac and serum creatinine levels, and compared pathological findings. Results: Daily doses were higher in the Tac-QD group, but trough levels and serum creatinine levels were comparable. On 3- and 12-month PB, the frequency of subclinical rejection was similar between the groups, while interstitial fibrosis and tubular atrophy (IF/TA) were less common in the Tac-QD group at 12 months (42.2% vs. 20.6%, P = 0.04). Univariate and multivariate logistic click here regression analyses revealed allograft rejection (borderline changes or higher) was associated with IF/TA (odds ratio 4.09, 95% confidence interval 1.76–10.10,

P = 0.001). The Tac-QD-based regimen showed a trend toward the absence of IF/TA but it did not reach statistical significance. Tubular vacuolization and arteriolar hyaline changes were also comparable in the two groups. Conclusion: We found a trend toward milder IF/TA, but no significant differences in kidney allograft pathology in patients treated with Tac-QD- versus Tac-BID-based regimens at 12 months. The effects of Tac-QD on chronic allograft injury need to be studied MS-275 ic50 by longer observation. FANG DOREEN YP1,2,

LU BO1, HAYWARD SUSAN3, DE KRETSER DAVID3, COWAN PETER1,2, DWYER KAREN1,2 1Immunology Research Centre, St Vincent’s Hospital Melbourne, Victoria, Australia; 2Department of Medicine, The University of Melbourne, Victoria, Australia; 3Monash Institute of Medical Research, Monash University, Victoria, Australia Introduction: Ischemia-reperfusion injury (IRI) accompanies organ transplantation causing inflammation and potentially contributing to poor graft function. Activin is a key driver of inflammation and it is regulated by follistatin. The aim of this study is to investigate the level of activin and the effect of follistatin treatment in renal IRI. Methods: Mice received 5 μg follistatin (n = 4) or

vehicle (n = 4) 30 mins before right nephrectomy and clamping of the left renal pedicle for 20 mins. A sham group (n = 6) GPX6 underwent right nephrectomy without clamping. Mice were sacrificed at 24 hrs. Serum was collected to measure activin A and B by ELISA. Serum creatinine was measured as a marker of renal function. Kidney sections were stained with H&E and scored to evaluate tubular injury on a scale of 0–4. Real-time PCR was performed to analyze the mRNA expression of IL-1β, IL-6, TNFα and kidney injury molecule-1 (KIM-1). Results: Renal IRI increased serum activin A, activin B, creatinine, tubular injury score, and mRNA expression of IL-1β, IL-6, TNFα and KIM-1. Follistatin treatment prior to ischemia reduced activin A, activin B, creatinine, and mRNA expression of IL-6 and KIM-1. There was a trend of improvement in tubular injury score, and mRNA expression of IL-1β and TNFα. [Table 1] Conclusion: Activin is upregulated during renal IRI.