Keane W F, Kasiske B L, O'Donnell M P
Department of Medicine, University of Minnesota Medical School, Minneapolis 55415.
Am J Clin Nutr. 1988 Jan;47(1):157-60. doi: 10.1093/ajcn/47.1.157.
Focal glomerulosclerosis (FGS) is commonly seen in human and in experimental models of chronic renal disease. Although considerable experimental data suggest that hypertension is important in progressive nephron damage, recent studies also have indicated that abnormal lipid metabolism may be an independent risk factor in the pathogenesis of FGS. Indeed, the synergistic impact of hypertension and hyperlipidemia in the pathogenesis of FGS may be analogous to the role of these factors in the pathogenesis of atherosclerosis. This review focuses on some of the recent and pertinent data that support a role of lipid-mediated glomerular injury in the pathogenesis of progressive renal disease.
局灶节段性肾小球硬化(FGS)常见于人类慢性肾病及相关实验模型中。尽管大量实验数据表明高血压在进行性肾单位损伤中起重要作用,但近期研究也表明,异常脂质代谢可能是FGS发病机制中的一个独立危险因素。事实上,高血压和高脂血症在FGS发病机制中的协同作用可能类似于这些因素在动脉粥样硬化发病机制中的作用。本综述聚焦于一些最新的相关数据,这些数据支持脂质介导的肾小球损伤在进行性肾病发病机制中的作用。