Warwick G L, Caslake M J, Boulton-Jones J M, Dagen M, Packard C J, Shepherd J
Department of Pathological Biochemistry, Glasgow Royal Infirmary, United Kingdom.
Metabolism. 1990 Feb;39(2):187-92. doi: 10.1016/0026-0495(90)90074-m.
Hyperlipidemia is a consistent feature of the nephrotic syndrome. In this study, low-density lipoprotein (LDL) metabolism has been investigated in nine patients with nephrotic syndrome and varying degrees of proteinuria. In subjects with moderate proteinuria (less than 10 g/d), total plasma cholesterol values were elevated to approximately 160% of normal due mainly to an increase in circulating LDL cholesterol. Metabolic studies showed that a defect in LDL clearance via the receptor pathway was responsible for its accumulation. The total amount of LDL apolipoprotein catabolized by this mechanism was only 55% of the value seen in controls; 60% more LDL was channelled into alternative, receptor-independent, catabolic pathways. Heavier proteinuria was associated with substantial increases in plasma triglyceride and very-low-density lipoprotein (VLDL) levels. The defect in LDL catabolism was aggravated by oversynthesis of the lipoprotein, which expanded the plasma LDL pool to 250% of normal. These observations indicate that the hyperlipidemia of the nephrotic syndrome is multifactorial in origin. The altered catabolism of LDL may be important in predisposing these subjects to premature atherosclerosis.
高脂血症是肾病综合征的一个持续特征。在本研究中，对9例患有肾病综合征且蛋白尿程度不同的患者进行了低密度脂蛋白（LDL）代谢研究。在中度蛋白尿（低于10 g/d）的受试者中，血浆总胆固醇值升高至正常水平的约160%，主要是由于循环中的LDL胆固醇增加。代谢研究表明，通过受体途径清除LDL存在缺陷是其蓄积的原因。通过该机制分解代谢的LDL载脂蛋白总量仅为对照组的55%；60%以上的LDL进入了替代性的、不依赖受体的分解代谢途径。蛋白尿较重与血浆甘油三酯和极低密度脂蛋白（VLDL）水平大幅升高有关。脂蛋白过度合成加剧了LDL分解代谢的缺陷，使血浆LDL池扩大至正常水平的250%。这些观察结果表明，肾病综合征的高脂血症起源是多因素的。LDL分解代谢改变可能在使这些受试者易患早发性动脉粥样硬化方面起重要作用。
