Lipid deposition, mononuclear cell infiltration and accumulation of mesangial matrix components are recognized as early events in the development of glomerulosclerosis whilst correction of plasma lipid abnormalities slows the progression of renal disease in experimental models. In vitro studies have demonstrated that low density lipoprotein (LDL) is bound and internalized by mesangial cells, acts synergistically with growth factors to stimulate cellular proliferation and modifies secretion of chemotactic mediators and matrix components. LDL incubated with mesangial cells becomes oxidized and in this modified from inhibits cell proliferation and causes cytotoxic injury. Oxidation of LDL also modulates its effects on cell secretory function. Since proteoglycans secreted by mesangial cells bind LDL particles, excess matrix accumulation may exacerbate lipoprotein-mediated injury. These findings suggest that lipoproteins deposited and oxidized in the glomerulus may promote inflammation, cell injury and sclerosis.