*2.8. FGF23*

FGF23 is a phosphaturic hormone primarily secreted by osteocytes. Its main actions are maintaining phosphate and mineral homeostasis. Furthermore, FGF23 decreases the synthesis of calcitriol. Its level rises early and dramatically with the decline of kidney function [51]. FGF23 has e ffects on various organs. Numerous studies have shown a correlation between serum FGF23 and cardiac alterations in CKD patients [52–58]. FGF23 directly induces LVH independent of preserved or reduced renal

function; this has been shown in vitro in cultured cardiomyocytes and by in vivo studies in mice, as well as by correlations of circulating FGF23 levels with LVH in CKD patients [55]. FGF23 stimulates pro-fibrotic and pro-hypertrophic factors in cardiomyocytes and induces fibrosis-related pathways in fibroblasts [55,59,60]. In addition to its direct e ffects on cardiac remodeling, FGF23 has also been shown to increase blood pressure [61], inflammation [62] and CKD progression itself [63], and may thus promote the development of LVH also by indirect mechanisms. FGF23 signaling in the liver causes production of inflammatory cytokines. In the bone, FGF23 inhibits mineralization, leading to increased circulating phosphorus levels while reducing the production of erythropoietin (EPO) in the bone marrow [64]. All of the above-mentioned actions a ffect the outcome of CKD patients, and thus directly or indirectly lead to progression of cardiovascular disease.
