Glomerular atherosclerosis.

Abstract

This paper suggests a two-hit model for lipoprotein-mediated progressive renal disease, in which postsecretory modification of low-density lipoprotein may favour the transformation of mesangial cells, monocytes and macrophages to glomerular foam cells. Proteinuria and lipiduria would mediate tubulointerstitial damage. Based on this, careful treatment with lipid-lowering agents, lipopheresis and antioxidants may ameliorate the progression of glomerular and tubulointerstitial pathology.