Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 365-375 |
| Number of pages | 11 |
| Journal | American Journal of Nephrology |
| Volume | 13 |
| Issue number | 5 |
| DOIs | |
| State | Published - 1993 |
All Science Journal Classification (ASJC) codes
- Nephrology
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