The majority of transplants are derived from donors who suffered from brain injury. There is evidence that brain death causes inflammatory changes in the donor. To define the impact of brain death, we evaluated the gene expression of cytokines in human brain dead and ideal living donors and compared these data to organ function following transplantation.Hepatic tissues from brain dead (n = 32) and living donors (n = 26) were collected at the time of donor laparotomy. Additional biopsies were performed before organ preservation, at the time of transplantation and one hour after reperfusion. Cytokines were assessed by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and cytometric bead array. Additionally, immunohistological analysis of tissue specimens was performed. Inflammatory cytokines including IL-6, IL-10, TNF-a , TGF-b and MIP-1a were significantly higher in brain dead donors immediately after laparotomy compared to living donors. Cellular infiltrates significantly increased in parallel to the soluble cytokines IL-6 and IL-10. Enhanced immune activation in brain dead donors was reflected by a deteriorated I/R injury proven by elevated alanin-aminotransferase (ALT), aspartat-amino-transferase (AST) and bilirubin levels, increased rates of acute rejection and primary nonfunction. Based on our clinical data, we demonstrate that brain death and the events that †Authors contributed equally to this manuscript.precede it are associated with a significant upregulation of inflammatory cytokines and lead to a worse ischemia/reperfusion injury after transplantation.

Our present study verifies the protective effect of methylprednisolone treatment in deceased donor liver transplantation, suggesting it as a potential therapeutical approach.

No abstract

Body:The matching was performed on 1300 kidney transplants from a single center population of transplants between 1996 and 2001. When samples were taken singly from 0 to 6 mismatch, there was an increased graft survival for each match grade examined. Most commonly, differences were more pronounced with time, however, 0,1,2 mismatch groups had smaller numbers. Therefore, 0,1,2 mismatch were combined as Group I and Ͼ2 mismatch as Group II. We found approximately 2% increase in graft survival per year for Group I as compared to Group II. This 2% was additive over the first 5 years examined. Interestingly, we could show that Group I was associated with lower average trough level for both immunosuppressed groups (neoral and tacrolimus). This was empirical and not done with any prospective immunosuppressive protocol. Furthermore, the patient survival was higher in Group I (pϭ.001). Conclusion: Matching from a single large center has shown efficacy at comparing 0,1,2 mismatches to Ͼ2 mismatch. Patient survival and lower immunosuppression was indicative of shorter hospital stay, less rejection, and fewer complications.Aims: Since Sept. 20, 1999 our organ procurement organization (OPO) that serves an ethnically diverse local distribution area has allocated kidneys from deceased donors using a UNOS approved kidney allocation variance that awards 7 points for a 0-CREG,0-DR mismatch (MM) and 6 points for a 0-A,B MM. Points were also given for waiting time (3) and panel-reactive antibodies (PRA) Ͼ80% (3). Previously we showed that awarding points for 0-CREG,0-DR MM in kidney allocation improves the access to HLA matched transplants for all racial groups, especially the black race. In this study we evaluated if there are graft outcome benefits as well. Methods: One and 3 year uncensored graft survival (GS) data were provided by Scientific Registry of Transplant Recipients (SRTR) and analysed for the influence of HLA mismatching on graft outcome in black and non-black recipients. Results: Overall, 1 year GS was 87.4% (Nϭ1,197) and not significantly different for blacks (86.1%, Nϭ467) and non-blacks (88.2%, Nϭ730); 3 year GS was 74.6% (Nϭ1,245) and significantly lower for blacks (68.5%, Nϭ480) vs. non-blacks (78.4%, Nϭ765), pϭ0.0001. * ϭ less than 30 cases No significant improvement in GS (pϭNS) was seen with HLA matching, including 0-CREG, 0-DR MM, for either the black or non-black recipients (Table) and also not seen when data was stratified for patients non-sensitized (PRAՅ10%) and sensitised (PRA Ͼ10%) at the time of transplant. Of those relisted after a failed graft, the 0-A,B,DR MM group was the least sensitized (6%, Nϭ16) as expected, and there was a trend for less sensitization in the 0-CREG,0-DR MM group (33%, Nϭ9), compared to those with other HLA mismatches (67%, Nϭ126). Conclusions: In conclusion, based on 1-year and 3-year follow-up data, there are no apparent graft oucome benefits for either CREG matching or conventional HLA matching in our service area. Such benefits may become apparent with longer follow-up.