[Pathomechanism of the development of chronic obliterative transplantation arteriopathy in human kidney allografts].

Authors examined cells participating in intimaproliferation in transplantation arteriopathy ultrastructurally in needle and wedge biopsy material from 40 transplanted kidneys, and immunohistochemically in 10 cases. In early biopsies--even in two control kidneys--it could be observed that the smooth muscle cells of media are in direct contact with endothel cells by their small processes. Processes can fulfil a receptor function and can transmit endothel noxa to smooth muscle cells. Smooth muscle cells of media react to endothel damage caused by rejection with migration to intima and during this period they are transformed to myofibroblasts (myointimal cells). In the mean time inflammatory cells (mainly macrophages, helper and cytotoxic cells in lower number) from the lumen infiltrate the intima, and mediators, enzymes released from them can inspire smooth muscle cells to further proliferation, migration to intima and transformation to myofibroblast. To effect of mediators (gamma interferon) released from inflammatory cells, the myointimal cells during rejection will press out 2nd class transplantation antigens (HLA-DR), and as vicious circle it further aggravates immune reply to graft, causing vascular damage, intimaproliferation.