Abrass Christine K
Department of Medicine, University of Washington School of Medicine, Seattle, Wash., USA.
Contrib Nephrol. 2006;151:106-121. doi: 10.1159/000095323.
Metabolic syndrome is associated with dyslipidemia, which is thought to contribute in part to the development of chronic kidney disease (CKD). This review discusses the factors that regulate intracellular handling of lipids and their relationship to disordered mesangial cell function. Specific attention is paid to those factors such as fatty acid translocase/scavenger receptor BII, proliferator-activated receptor delta, insulin-like growth factor-1, inflammation and hypertriglyceridemia that are altered in the metabolic syndrome. CKD also causes an increase in triglycerides and a decrease in high-density lipoprotein that mimic the lipid abnormalities of metabolic syndrome, which accelerate the progression of CKD and increase the risk for cardiovascular mortality. There is a special emphasis on foam cells in the kidney and lipid-mediated changes in intrinsic kidney cells that lead to glomerulosclerosis and interstitial fibrosis. Correlates to whole animal and humans studies are included.
代谢综合征与血脂异常有关,血脂异常被认为在一定程度上促成了慢性肾脏病(CKD)的发展。本综述讨论了调节细胞内脂质处理的因素及其与系膜细胞功能紊乱的关系。特别关注那些在代谢综合征中发生改变的因素,如脂肪酸转运蛋白/清道夫受体BII、增殖激活受体δ、胰岛素样生长因子-1、炎症和高甘油三酯血症。CKD还会导致甘油三酯升高和高密度脂蛋白降低,这与代谢综合征的脂质异常相似,会加速CKD的进展并增加心血管死亡风险。本文特别强调了肾脏中的泡沫细胞以及导致肾小球硬化和间质纤维化的肾脏固有细胞中的脂质介导变化。文中还纳入了与整体动物和人体研究的相关性内容。