Estradiol and follicle-stimulating hormone imbalance associated with mineral-bone metabolism disturbances and cardiovascular complications in women on hemodialysis

Abstract

BACKGROUND. The influence of female sex hormones on the regulation of the processes of formation and resorption of bone tissue, as well as the effect of excess or deficiency of sex hormones on renal function is associated with the development of cardiovascular complications in patients at different stages of chronic kidney disease. THE AIM : to study the relationship between estradiol deficiency and excess FSH content with disorders of mineral and bone metabolism and cardiovascular complications in postmenopausal women on hemodialysis. PATIENTS AND METHODS. 119 women from 34 to 57 years old on hemodialysis were examined. The concentration of follicle-stimulating hormone (FSH) and estradiol2, sclerostin, and fibroblast growth factor 23 (FGF-23) was determined using a sandwich-variant solid-phase ELISA on a «Multiscan EX analyzer» («ThermoFisher Scientific Inc.», Finland) with kits of «Alkor-Bio Company» (Russian Federation) and sets of "sandwich" type manufactured by Cloud-Clone Corp., USA. Echocardiography was performed using an «ALOKA 4000 Aplio» (Toshiba, Japan) in Doppler mode. Determined the left ventricular ejection fraction (LVEF), peak systolic velocity in the aortic arch (Vps – peak systolic velocity); LV myocardial mass index (LVMI). Left ventricular hypertrophy (LVH) was defined with LVMI greater than 95 g /m 2 in women. RESULTS. There was a direct correlation between high levels of FSH and high levels of sclerostin, FSH, and FGF23, an inverse correlation between low levels of estradiol2 and sclerostin, estradiol2 and FGF23, expressed in groups of patients with more severe changes in LVMI and Vps. CONCLUSION. In women on hemodialysis, bone mineral and cardiovascular abnormalities are associated with both renal failure proper and changes in the system of female sex hormones. A decrease in estradiol levels causes an increase in the nephrotoxic FSH and contributes to the excessive synthesis of sclerostin, a key factor in bone-mineral and cardiovascular complications in CKD.