The role of sclerostin in the formation of cardiovascular calcifi cation in chronic kidney disease C5D

Abstract

THE AIM: to study the relationship of blood sclerostin with clinical parameters and its influence on the probability of detection of cardiovascular calcification in patients with CKD C5D.PATIENTS AND METHODS. The study was a single-stage, cohort study involving 84 patients with stage 5D CKD who received hemodialysis therapy, including 40 (47.6 %) female patients and 44 (52.4 %) male patients. The average age was 55.6±14.9 years. The examination included, in addition to routine studies, echocardioscopy with an assessment of calcification of the heart valves, abdominal radiography in the lateral projection with an assessment of aortic calcification, analysis of indicators that characterize phosphorus-calcium metabolism (serum sclerostin levels, 1.25(OH)D, FGF-23, A-klotho, PTH, P and Cа blood). Statistical analysis was performed using the computer program STATISTICA 12.6 (StatSoft Inc., USA).RESULTS. It was shown that the level of sclerostin is higher in the elderly, as well as those who have signs of hypoproteinemia and hypoalbuminemia, indirectly indicating the presence of protein-energy deficiency. There is an Association of blood sclerostin with FGF-23 and Alpha-klotho. From the point of view of the probable influence on the processes of cardiovascular calcification, this relationship shows its unidirectionality. Increased blood sclerostin levels have been shown to be associated with the risk of detecting signs of cardiovascular calcification. Moreover, it is shown that the higher the level of sclerostin in the blood, the more pronounced the degree of this calcification. Along with the increase in the level of sclerostin, the ability of a deficit of 1.25(OH)D to lead to the development of calcification was confirmed.CONCLUSION. A high level of sclerostin in the blood serum of more than 92.5 pmol / l in patients with CKD C5D increases the risk of detecting signs of cardiovascular calcification (calcification of the aortic wall and heart valves). An increase in sclerostin levels occurs in conjunction with an increase in FGF-23 and a decrease in 1.25(OH)D