The histopathologic features of CAN can be characterized by proliferative changes of the vascular wall, in which smooth muscle cells and parenchymal cells proliferate, leading to a narrowing of renal arteries, which may contribute to a relative hypoxia of the tissue. Subsequently, fibroblasts will contribute to fibrotic scarring in the vascular wall. CAN is also characterized by the occurrence of fibrosis in the interstitial tissue along with tubular atrophy (14). The glomeruli are also often affected by various degrees of glomerulosclerosis. An inflammatory infiltrate is frequently found and consists of invading lymphocytes and monocytes-macrophages into virtually all affected compartments of the kidney. The inflammatory infiltrate observed in CAN can be induced by both antigen-dependent and antigen-independent factors. These histopathologic changes can be graded according to the Banff system (14), which gives a score of the degree of CAN. These histopathologic changes act in concert, contributing to a gradual progression of renal allograft dysfunction.