Glomerular atherosclerosis.
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.
Moorhead
J F
JF
Department of Nephrology, Royal Free Hospital, Hampstead, London, UK.
Brunton
C
C
Varghese
Z
Z
D001161:Arteriosclerosis / Q000209:etiology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006949:Hyperlipidemias / Q000628:therapy; D007676:Kidney Failure, Chronic / Q000150:complications*; D008074:Lipoproteins / Q000502:physiology; D008077:Lipoproteins, LDL / Q000378:metabolism; D009404:Nephrotic Syndrome / Q000150:complications / Q000503:physiopathology; D010084:Oxidation-Reduction
D008074:Lipoproteins; D008077:Lipoproteins, LDL