Chronic renal transplant loss

Ever since the inception of kidney transplant programs the short-term patient and graft survival results have improved progressively, principally because of better management of acute rejection episodes and decreased mortality from infectious complications. However, the rate of annual graft attrition after the first post-transplant year has virtually remained unchanged [1, 2]. About half to three quarters of the late graft losses are explained by patient death with a functioning transplant, mainly as a result of cardiovascular causes, while chronic rejection accounts for 50 to 80% of graft failures in surviving recipients. The estimated graft loss from chronic rejection varies between 4 and 40% in the initial five post-transplant years [3]. Recent clinical [3] and experimental [4] studies have shown that acute rejection episodes are the most important risk factor for the development of chronic rejection, but their connection is currently unknown. Although immunological or "antigen-dependent" mechanisms are central in graft rejection, there is increasing evidence to support the hypothesis that non-immunological or "antigenindependent" mechanisms play a role in the progressive deterioration of structure and function late after transplantation. The importance of each of these components will be discussed following the description of the manifestations and risk factors of chronic rejection.