ABSTRACT

A number of insights noted years ago have supported a role for immunological events in chronic kidney graft failure. For example, HLA-identical kidney grafts enjoy a longer functional half-life.5 Even in the context of newer immunosuppressive strategies, at 10 years, 52% of HLA-matched grafts survive compared to only 37% of HLA-mismatched grafts.6 Secondly, acute rejection has been linked to chronic graft failure in kidney allografts, by a process called chronic allograft nephropathy (CAN).7 9 The impact of acute rejection on CAN has been rising despite use of newer immunosuppressants.10 Furthermore, there is improved graft survival for living related al­ lografts compared to cadaveric grafts.11,12 These clinical observations support the notion that immunological injury is a critical contributor to allograft failure.