30-P

Abstract

Inflammatory responses fundamentally influence the short and long term performance of organ transplantation. We think inflammatory markers released from the donor organ during organ procurement may trigger the innate immunity, causing cytokine production and alloreactive response to the donor organ which may initiate allograft dysfunction. It has been shown that an extended cold ischemic time or warm ischemia time during organ transplantation has been associated with increased risk of graft failure. In addition, increased inflammatory markers such as allograft inflammatory factor 1 (AIF-1) has been demonstrated in association with a poor outcome of allograft transplantation. We hypothesize that cold/warm ischemia time may increase the release of AIF-1 from the donor organ during procurement, stimulating innate immune effector-cells, and the production of inflammatory cytokines which may influence allograft function, causing a delayed graft function (DGF) and rejection episodes. In a preliminary study we assessed the impact of cold and warm ischemia time on the clinical outcomes in patients that had undergone renal allograft transplantation. In addition, expression levels of AIF-1 mRNA in the peripheral blood mononuclear cells (PBMCs) were examined in association with cold ischemia time and DGF. The results were analyzed using one-way ANOVA to establish the association with AIF-1 production. Cold ischemia time (CIT) ⩽10 hours had less impact on DGF as compared with CIT⩾ 20 hours. Impact of the CIT ⩽ 10 was a 3.5-fold increase in patients who achieved GFR value ⌈ sup ⌉ ⩾ ⌈ / sup ⌉ 55 within the first week after transplantation as compared to CIT ⩾ 20, p < 0.04. Cold and warm ischemia time inversely has impact in the outcome of allograft function determined by the value of GFR. AIF-1 mRNA was significantly increased in the CIT ⩾ 20 as compared with CIT ⩽ 10. Cold and warm ischemia/repefusin time inversely have impact on the outcome of allograft function. AIF-1 expression was increased with CIT ⩾ 20.