论文部分内容阅读
目前糖尿病肾病(Diabetic Nephropathy, DN)的发病机制仍不完全清楚,一般认为与代谢紊乱,血流动力学改变和微血管病变有关。但近年来,国外有学者发现DN的发病存在自身免疫证据。 1 一般发病机制 1.1 代谢紊乱 1.1.1 多元醇代谢通路活性增高:长期高血糖状态,可激活葡萄糖的多元通路,使醛糖还原酶活性升高,组织细胞内较多的葡萄糖被醛糖还原酶催化还原为山梨醇,山梨醇必须经脱氢酶转化为果糖方能逐渐氧化,糖尿病时该酶活性降低,使细胞内山梨醇和果糖积聚增多,且由于山梨醇能吸水而使细胞肿胀变性,功能受损。
At present, the pathogenesis of Diabetic Nephropathy (DN) is still not fully understood, and it is generally considered to be related to metabolic disorders, hemodynamic changes and microangiopathy. However, in recent years, foreign scholars found that there is evidence of autoimmunity in the pathogenesis of DN. 1 General pathogenesis 1.1 Metabolic disorders 1.1.1 Polyol metabolic pathway activity increased: long-term hyperglycemic state, can activate multiple channels of glucose, aldose reductase activity increased, more cells within the cells by glucose aldose reductase Catalytic reduction of sorbitol, sorbitol must be dehydrogenase into fructose can be gradually oxidized, reducing the enzyme activity in diabetes, the accumulation of intracellular sorbitol and fructose increased, and as sorbitol water swelling and cell swelling and degeneration, function Damaged.