PATHOPHYSIOLOGICAL MECHANISMS OF DEVELOPMENT OF CHRONIC KIDNEY DISEASE IN POSTMENOPAUSAL WOMEN
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Abstract
Chronic kidney disease (CKD) is a global health problem characterized by a progressive decline in kidney function. The contribution of women to the general population of patients with CKD is significant, and, importantly, postmenopausal women experience accelerated progression of this disease. The purpose of the review is to analyze current literature sources on the mechanisms of development of acute and chronic kidney injury in postmenopausal women and the possibility of correcting disorders. Materials and methods. The methodological approaches used to achieve this goal are based on the study of more than 40 literature sources, of which 19 articles are included in the review. Results. The development of CKD in postmenopausal women is a complex and multifactorial process caused by the interaction of hormonal, vascular, inflammatory, and metabolic factors. After menopause, a decrease in estrogen levels leads to a decrease in the synthesis of nitric oxide, a powerful vasodilator, and an increase in the production of vasoconstrictor substances such as endothelin-1. This imbalance leads to increased vascular resistance in the kidneys, ischemia, and glomerulosclerosis. Activation of the RAAS also plays an important role in the development of CKD in postmenopausal women. Estrogens have an inhibitory effect on the RAAS by suppressing the synthesis of renin and angiotensin II. Conclusion. In conditions of estrogen deficiency, the RAAS is activated, which leads to an increased level of angiotensin II. A decrease in estrogen levels is a trigger that leads to activation of the RAAS, oxidative stress, inflammation, and impaired calcium metabolism, which ultimately contributes to kidney damage and the progression of CKD. Further research aimed at a deeper understanding of these pathophysiological mechanisms is necessary to develop effective strategies for the prevention and treatment of CKD in postmenopausal women, including the use of hormone replacement therapy, RAAS inhibitors, antioxidants and anti-inflammatory drugs, as well as the correction of metabolic disorders.
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