Chronic allograft nephropathy (CAN) is a devastating complication of kidney transplantation that is responsible for a significant proportion of graft loss (1-5). Although currently available immunosuppressive therapy is increasingly effective against acute rejection of a transplanted organ, chronic rejection (CR) remains difficult to treat. Nevertheless, a relevant proportion of patients with CR of a kidney transplant maintain satisfactory organ function for a long time. CAN is characterized by a progressive decline in kidney function, which is not attributable to a specific cause (6-8). CAN is a poorly known complex process resulting from as yet undefined etiology with both immune and non-immune components (8). Alloantigen-dependent causes of CAN include acute rejection episodes, particularly multiple, late, or vascular acute rejection episodes (9-13). With the use of a new immunosuppressive regimen, the frequency of acute rejection episodes has become reduced, which may possibly have an influence on future development of CAN. However, donor antigen-independent factors also play a role in the occurrence and progression of CAN. This includes donor-related factors such as donor age and number of mismatch, which have an impact on late graft outcome (13). Donation-related circumstances, such as prolonged cold ischemia time, are associated with delayed graft function and related to poor late renal transplant results.