DYNAMICS OF ENDOTHELIAL DYSFUNCTION INDICATORS DURING THE TREATMENT OF STAGE II–III CHRONIC KIDNEY DISEASE OF DIABETIC AND NON-DIABETIC ETIOLOGY

Activation of lipid peroxidation leads to endothelial dysfunction and alters the balance between vasodilating and vasoconstricting substances. Adenosine is a metabolite of ATP that, in most cases, causes vasodilation, but in the kidneys it induces vasoconstriction, thereby increasing hypoxia. Nitric oxide is a vasodilator whose concentration in the renal parenchyma in diabetic nephropathy is partially reduced due to increased degradation of the molecule under the influence of free radicals in the absence of oxygen. Nitric oxide is converted into stable molecules of nitrates and nitrites, and therefore its vasodilatory capacity decreases. An additional factor in renal vasoconstriction is a decrease in prostaglandin expression. The activity of all the above vasoconstrictor factors increases, while vasodilatory factors decrease, leading to reduced oxygen concentration in the renal parenchyma.脂质过氧化（lipid peroxidation）的激活可诱发内皮功能障碍（endothelial dysfunction），并打破血管舒张物质与血管收缩物质之间的平衡。腺苷（adenosine）是三磷酸腺苷（ATP）的代谢产物，多数情况下可介导血管舒张，但在肾脏中却会诱导血管收缩，进而加剧组织缺氧。一氧化氮（nitric oxide）是一种血管舒张因子，在糖尿病肾病（diabetic nephropathy）患者的肾实质（renal parenchyma）中，由于缺氧状态下自由基（free radicals）的作用加速了该分子的降解，其浓度会出现一定程度的下降。一氧化氮会转化为稳定的硝酸盐（nitrates）与亚硝酸盐（nitrites）分子，因此其血管舒张能力随之降低。另一个引发肾脏血管收缩的因素是前列腺素（prostaglandin）表达量的下调。上述所有血管收缩因子的活性均会升高，而血管舒张因子的水平则出现下降，最终导致肾实质内的氧浓度降低。