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Rejection: An Integrated Response

Over the last four decades the strategies used to prolong graft survival in renal transplantation have been to avoid immune memory and to target T cells to prevent acute cellular rejection (TCMR). With modern crossmatch technologies and current immunosuppression we have successfully reduced acute rejection rates to 10–15% in the first year. Unfortunately this has translated into onlymodest improvement in long-term graft outcomes, and the evidence indicates that the immune system remains the major mediator of late graft loss (1–3). Specifically, the importance of chronic antibody mediated rejection (AMR) from de novo donor specific antibody (DSA) has come to the forefront while TCMR has largely been relegated to a minor role in effecting graft loss (3,4).