Vitamin E treatment of experimental glomerular disease in rats

Background Kidney mesangial cells (MCs) and vascular smooth muscle cells (V SMCs) are closely related in terms of origin, microscopic anatomy, histoche mistry, and contractility. This relationship suggests a similarity between kidney glomerular sclerosis and atherosclerosis. Vitamin E appears benefici al in the prevention and treatment of coronary heart disease and it also in hibits the proliferation of VSMCs in vitro. Thus, we investigated the effec t of vitamin E on glomerular sclerosis and MC-proliferative glomerulonephri tis (GN) in two rat models of glomerular disease. Methods. A remnant kidney rat model accelerated with hyperlipidemia was use d to examine progressive glomerular sclerosis leading to chronic renal fail ure. A rat model of MC-proliferative GN was induced by the intravenous admi nistration of absorbed rabbit anti-rat thymocyte serum (ATS). Results. In the remnant kidney rat model, dietary supplementation with vita min E (500 IU dl-alpha-tocopheryl acetate/kg) and cholesterol (2%) signific antly inhibited glomerular sclerosis and macrophage infiltration in glomeru li relative to controls receiving basal and cholesterol-supplemented diets. In the ATS-induced GN model, glomerular cell proliferation (principally MC s) was lower in rats fed diets supplemented with vitamin E (1000 IU dl-alph a-tocopheryl acetate/kg) compared with controls fed the basal diet only. Al though the degree of glomerular macrophage infiltration was similar in both groups, fewer proliferative cell nuclear antigen (PCNA)-positive cells wer e observed in the vitamin E group, suggesting that MC proliferation was sup pressed via the inhibition of intracellular transduction. Conclusions. Supplemental dietary vitamin E suppresses MC proliferation and glomerular sclerosis in models of glomerular disease in rats. This action of vitamin E in experimental nephritis suggests the value of clinical trial s testing the potential benefit of vitamin E in chronic GN patients.