2a). In the Pre + Post RBCT group the risk of AMR was 13.9 times greater in those patients with DSA than in patients with Non-DSA or No-Antibody (Fig. 2b p = 0.001). Indeed all 13 episodes of AMR in the DSA group occurred exclusively in patients who had received Pre + Post-RBCT. On the other hand, 0/6 patients with Non-DSA and 2/37 in the No-antibody group who had received Pre + Post-RBCT developed AMR. The median time between post-operative UK-371804 purchase transfusion and AMR in the DSA patients was 25 days (IQR 5–761 days). Univariate predictors of AMR were

pre-transplant DSA (HR 6.6 95%CI 2.9–14.7, p < 0.001), DGF (HR 2.6. 1.1–6.1, p = 0.039), re-transplant (HR 3.3 1.3–8.3 p = 0.024) and Pre + Post-RBCT (HR 4.1, 1.6–10.8 p = 0.005) but not females (HR 0.9 0.38–2.1). There was a significant interaction between Pre-RBCT and Post-RBCT (HR 4.4 2.0–9.8 p = 0.001) and between DSA and Post-RBCT (HR 10.6 4.7–23.8 p < 0.0001) on the risk of AMR. In a multivariate Cox model incorporating the above univariate factors and adding interaction terms, only the interaction between DSA KU-60019 mouse and Post-RBCT (HR 7.2, 2.9–18.0, p = 0.001)

remained a significant predictor of AMR. Death-censored graft loss (Fig. 3 and Table 3) and combined patient and graft loss (Table 3) was significantly increased in the Pre + Post-RBCT group (HR 7.1 p < 0.001) compared with all other transfusion groups. This difference persisted even after exclusion of the 37 patients with preformed DSA (HR 4.9 95% Histamine H2 receptor CI 1.5–15.8

p = 0.007 and 3.9 1.7–7.8 p = 0.001 respectively). Neither gender nor retransplant were associated with graft or patient loss. We used significant univariate predictors of graft loss including DGF, HLA antibody (DSA and Non-DSA), AMR and Non-AMR rejection and transfusion history in a multivariate Cox Proportional Hazards model (Table 3). AMR, Non-AMR rejection and Pre + Post RBCT were independently associated with death censored and all cause graft loss. However DGF and DSA were no longer predictive by multivariate analysis. We show that the risk of AMR associated with the presence of DSA at the time of transplant is modulated by exposure to RBCT. In our cohort, AMR was predominantly observed only in sensitised patients with DSA all of whom had received RBCT prior to transplant and were then transfused within the first 30 days (usually 48 h). Pre-transplant DSA and Pre + Post-RBCT were each independent predictors of AMR. However, there was a strong interaction between pre-transplant DSA and Post-RBCT, which eliminated all other predictors (DGF, re-transplant, gender), and conferred a 7.2 fold increase in the risk of AMR. In contrast, patients with DSA who received only Pre-RBCT or Post-RBCT, or who received no transfusion did not experience AMR. Overall, patients with DSA had the highest rate of post-operative transfusion.