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.

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