Abstract

Hyperhomocysteinemia is considered a risk factor for many diseases, including thrombosis. Patients with chronic kidney disease often have vascular complications in the form of arterial or venous thrombosis, and it is important to consider the blood homocysteine level as a predictor of thrombophilia. The causes of hyperhomocysteinemia can be both genetic mutations and deficiency of homocysteine metabolism enzymes, as well as deficiency of folic acid, vitamin B12 and, to a lesser extent, deficiency of vitamin B6, which affects methionine metabolism. Given the role of hyperhomocysteinemia as a predictor of cardiovascular events in patients with kidney diseases, in our opinion, the multifactorial nature of increased homocysteine requires further research into some links of its pathogenesis in chronic kidney disease and the development of targeted therapeutic interventions.

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