Решение кардиоваскулярных проблем у пациентов на диализе - акцент на коррекцию гиперфосфатемии

Mineral-bone disorder in chronic kidney disease (CKD-MBD) is one of the most important factor determining prognosis in dialysis patients. CKD-MBD syndrome occurs at the CKD stage 2 and reaches its maximum in patients with end-stage renal disease. Currently, hyperphosphatemia plays a central role in the pathogenesis of CKD-MBD(the so-called “phosphate-centric paradigm”). In turn, hyperphosatemia leads to an increase in the level of phosphaturic hormone - fibroblast growth factor type 23 (FGF23). FGF23 causes remodeling and fibrosis of the myocardium, renal parenchyma, the development of calcification and vascular atherosclerosis. Thus, hyperphosphatemia, indirectly, through an increase in the level of FGF23, is one of the most important manifestation of progressive CKD and a significant factor of high overall and cardiovascular morbidity and mortality in this cohort of patients. Given that cardiovascular events are the main cause of mortality in patients on renal replacement therapy with dialysis, correction of hyperphosphatemia is a prerequisite for successful monitoring of this group of patients and influencing prognosis. The review presents the main approaches for the correction of hyperphosphatemia in CKD, such as nutritional correction, modification of dialysis methods, and prescribing of phosphate binders. The advantages of calcium-free phosphate-binding agents are considered in details and had compared with effects of containing calcium phosphate binders. The treatment of hyperphosphatemia should be approached comprehensively, using optimal dialysis therapy regimens, training and monitoring dietary phosphate consumption with the obligatory use of phosphate binders that are most effective and well tolerated.