Biomarkers of heart and vascular lesions in the framework of mineral and bone disorders in chronic kidney disease, correction possibilities

Сardiovascular disease (СVD) is the most common complication of chronic kidney disease (СKD). In patients with the earlier stages of CKD, the risk of death from CVD greatly exceeds the risk of progression to end-stage renal disease. In recent years, accumulated data suggest that chronic kidney disease — mineral and bone disorders (CKD-MBD) are strongly associated with cardiovascular events and mortality. Among cardiovascular damage in CKD, both, the progressive cardiac remodeling and vascular calcifi cation, contribute immensely, and lead to an urgently high cardiovascular mortality in patients with CKD. Clarifi cation of CKD progression mechanisms and possible early markers of CVD has led to interest in studying the identifi ed factors such as fi broblast growth factor-23 (FGF-23), Klotho and sclerostin in recent years. Results of studies show that disorders in the system of FGF-23–Klotho–sclerostin correlate with the frequency and severity of hypertension, cardiac remodeling, vascular calcifi cation, anaemia, malnutrition, infl ammation, and strongly aggravate cardiovascular risk in CKD. This review represents an analysis of the available data showing the potential association of СVD with established (phosphate, parathyroid hormone (PTH), Vitamin D) and newer (FGF-23, Klotho, sclerostin) СKD-MBD biomarkers. In addition, it has been shown that renoprotective therapy, including renin-angiotensin blockers, low-protein diet with amino/keto acid supplementation, phosphate binders, erythropoiesis stimulators, vitamin D metabolites used to reach the target levels of blood pressure, serum phosphorus, haemoglobin, PTH and nutritional status disorders, can aff ect CKD-MBD biomarkers and reduce the risk of cardiovascular events in CKD patients.

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