Attman P O, Alaupovic P
Department of Nephrology, University of Göteborg, Sweden.
Am J Nephrol. 1990;10 Suppl 1:69-75. doi: 10.1159/000168197.
Both increased synthesis and decreased clearance of lipoproteinemia may contribute to the hyperlipoproteinemia which frequently complicates the nephrotic syndrome with increased levels of total and low-density lipo-protein (LDL) cholesterol as the most characteristic abnormality. The hyperlipoproteinemia may also be characterized by elevated levels of triglycerides, increased concentrations of Apo B, Apo C and Apo E and reduced levels of Apo A-I and Apo A-II. The increased lipoprotein synthesis occurs in partly undefined mechanisms related to proteinuria, hypoalbuminemia and, possibly, increased availability of mevalonate as a substrate for cholesterol synthesis. Urinary loss of high-density lipoprotein (HDL) components and other liporegulatory factors may contribute to decreased activity of lipolytic enzymes and result in impaired clearance of cholesterol- and triglyceride-rich lipoproteins of lower densities and altered composition of HDL. The variability in these two metabolic abnormalities may account for the corresponding variability in lipoprotein profiles of patients with the nephrotic syndrome.
脂蛋白血症的合成增加和清除减少均可能导致高脂蛋白血症，高脂蛋白血症常使肾病综合征复杂化，其最典型的异常表现是总胆固醇和低密度脂蛋白（LDL）胆固醇水平升高。高脂蛋白血症的特征还可能包括甘油三酯水平升高、载脂蛋白B、载脂蛋白C和载脂蛋白E浓度增加以及载脂蛋白A-I和载脂蛋白A-II水平降低。脂蛋白合成增加部分是通过与蛋白尿、低白蛋白血症相关的未明确机制发生作用，可能还与作为胆固醇合成底物的甲羟戊酸可用性增加有关。高密度脂蛋白（HDL）成分及其他脂质调节因子的尿中丢失，可能导致脂解酶活性降低，并致使密度较低、富含胆固醇和甘油三酯的脂蛋白清除受损以及HDL组成改变。这两种代谢异常的变异性，可能解释了肾病综合征患者脂蛋白谱的相应变异性。
