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.
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