To observe the histopathological changes of obliterative arteriopathy (OBA) in human renal allografts, analyse OBA cellular components and probe its pathogenesis.74 renal allografts removed due to acute vascular rejection and chronic rejection were studied by light microscopy, electron microscopy and immunohistochemistry methods.OBA predominately affected the intima of interlobar, arcuate and interlobular arteries in all the 74 renal allografts. 29 cases developed OBA within 3 months post transplantation. 19 (25.7%) renal allografts showed early OBA with intimal arteritis, 55 (74.3%) cases had advanced OBA with intimal spindle-shaped smooth muscle cell (SMC) proliferation and intimal fibrosis. The cellular composition of OBA consisted of two origins, one from the host and the other from arterial wall intrinsic cells of renal allografts, including T lymphocytes; monocyte/macrophage cells; endothelial cells and different phenotypes--"contractile" or "synthetic" SMCs, "synthetic" SMCs secreted collagen types I, III.Our findings suggest that OBA is a post transplantation intrarenal arterial wall proliferative lesion. It is the result of a series of interactions between host immunocytes and allograft vascular wall cells. OBA is a type of immune reaction.