Avram M M
Long Island College Hospital, Division of Nephrology, Brooklyn, New York 11201.
Am J Med. 1989 Nov;87(5N):39N-41N.
Much recent work has focused on the progressive nature of renal injury, and hemodynamic alterations have been implicated in the pathogenesis of the predominant lesion, focal glomerulosclerosis. Despite the well-documented atherogenic toxicity of lipids in cardiovascular morbidity, little is known about lipid-associated renal injury. However, lipids are toxic to endothelium, and the glomerulus is a vascular bundle. Several authors participating in this symposium have presented evidence for an association between hyperlipidemia and glomerulosclerosis in animal models. This association is particularly significant given the expanded therapeutic armamentarium now available to treat hyperlipidemia. In fact, glomerular injury may be moderated by pharmacologic treatment of hyperlipidemia in a rat renal ablation model. Very little evidence exists, however, for a similar association in human renal disease. We have, in the course of clinical practice, made certain observations in renal biopsy specimens that may for the first time link atherogenesis and lipid deposition to human glomerular injury.