Relationship between hyperlipidemia, lipid mediators, and progressive glomerulosclerosis in the nephrotic syndrome.

Nephrotic syndrome is defined by proteinuria, hypoalbuminemia, edema and hypercholesterolemia. Evidence from both the experimental and clinical literature suggests that high lipid levels are not only a marker of disease, but also contribute to the process of glomerulosclerosis. Lipid mediators, including eicosanoids, platelet-activating factor, and chemotactic factors, can contribute by effecting leukocyte infiltration, mesangial proliferation, extracellular matrix protein production, vasoreactivity, and coagulation. Infiltrating macrophages may play a central role in these processes. Therapeutic maneuvers aimed at the correction of lipid abnormalities may halt or slow the progression of nephrotic syndrome to end-stage renal disease.