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The chapter discusses the current understanding of the system of mineral and bone metabolism regulators—FGF-23, Klotho and sclerostin—disturbances in chronic kidney disease (CKD). In the chapter we presented the date, including our own results, which allow to suggest the change in the ratio of FGF-23-Klotho-sclerostin in CKD as an early biomarker not only for the chronic kidney damage but also for high cardiovascular (CV) risk. Results of studies show that disorders in FGF-23-Klotho-sclerostin ratio correlate with the frequency and severity of hypertension, vascular calcification, cardiac remodelling, anaemia, malnutrition, inflammation and strong aggravate CV risk in CKD. It was found independent from blood pressure (BP) action of increased serum FGF-23 on the myocardium as well as the correlation of serum high-sensitive troponin I with increased serum FGF-23 and low Klotho levels in CKD patients. At the same time, it was shown that renoprotective therapy, including renin-angiotensin blockers, low-protein diet with amino/keto acid supplementation and phosphate binders, erythropoiesis stimulators, vitamin D metabolites used to get the target levels of BP, serum phosphorus, haemoglobin, parathyroid hormone and nutritional status disorders correction can reduce the risk of CV events, as the major cause of death in CKD patients.

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Disorders in the System of Mineral and Bone Metabolism Regulators—FGF-23, Klotho and Sclerostin—in Chronic Kidney Disease: Clinical Significance and Possibilities for Correction