Stevenson F T, Kaysen G A
Department of Medicine, University of California, Davis School of Medicine, USA.
Wien Klin Wochenschr. 1999 Apr 23;111(8):307-14.
Hyperlipidemia accelerates the progression of human renal disease, and its control is becoming an important component of therapy for patients with renal failure. The biologic basis for these observations remains poorly understood. This review summarizes recent data from animal models which show how lipoproteins interact with cells directly to cause renal injury. Data are presented from recent studies on the obese Zucker rat, a metabolic model of hyperlipidemia, obesity, and glomerular sclerosis, showing that triglyceride-containing lipoproteins may mediate glomerular injury. The biochemical basis for therapy is also discussed, including actions of lipid-lowering agents apart from their effect on serum lipids, and the use of polyunsaturated fatty acids as dietary therapy. Animal models are a crucial tool for the further elucidation of mechanisms of lipoprotein-mediated glomerular injury.