Samples had been analyzed with a equivalent frequency in each groups with . and . samples per year of comply with up in the cyclosporine and everolimus arm, respectively p Formation of DSA Seven out of .% cyclosporine treated patients developed de novo DSA during a median Caspase molecular weight stick to up of days. DSA had been detected on median days soon after transplantation. A higher incidence of DSA was observed in patients randomized to everolimus %, Figure . Despite a equivalent follow up of days the time to first occurrence of DSA was shorter in comparison to the cyclosporine group , range days . All CyA individuals with de novo DSA formation developed DSA against HLA class II antigens. 1 patient additionally created a class I antibody Cw . Class II DSA were directed against DR in individuals,DQin individuals, and both DR and DQ in patient. All DSA had been detected sustained with mean fluorescence intensities MFI ranging from MFI to MFI and MFI to MFI for class Iand class II DSA, respectively. De novo DSA of everolimus treated patients had been directed exclusively against class I antigens in against HLA A B, against B , class II antigens in against HLA DQ, against DR and against DP , and both class I and IIantigens in individuals one against HLA A DR, A DQ along with a DR DQ each .
DSA of everolimus treated patients were detected sustained with MFI values of to and to for class I and class II DSA, respectively. Biopsy established AMR, graft losses and outcome Ten out of de novo DSA positive individuals created biopsy verified AMR Table . Eight individuals randomized to the everolimus based immunosuppression, and two with continued use of Bicalutamide cyclosporine log rank test: p Figure . Four with the eight everolimus individuals with AMR lost their graft regardless of intensive efforts to maintain kidney function. The kidney function of the other individuals with AMR is shown in Table . 3 extra graft losses had been observed in individuals without the need of AMR: two individuals within the cyclosporine group graft loss as a result of several infectious complications, and graft loss as a result of substantial interstitial fibrosis . One patient randomized to everolimus lost the graft due to recurrence of FSGS. Serum creatinine, proteinuria and graft and patient survival from the cohort are summarized in Table . Threat factors for DSA formation In order to further define danger variables for the formation of DSA we performed univariate regression analyses. Waiting time, immunosuppressive regimen by ITT , mismatches, living donors and treated acute rejections in the course of the initial year were identified as potential confounders p . in univariate regression analyses. Working with these possible danger components inside a multivariate backward elimination p . Cox regression model, only everolimus based immunosuppressive regimen, mismatches and graft from a living donor remained considerable threat variables related to de novo DSA formation Table .