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Regulation of mineral metabolism is a complex process, and our current models are constantly revised. The cloning and characterization of fibroblast growth factor-23 (FGF-23) has revolutionized our understanding of the endocrine regulation underlying phosphate and vitamin D metabolism. FGF-23 was initially regarded as a pathogenic factor primarily involved in hereditary skeletal disorders of hypophosphataemic rickets [1–3], however the area of research related to FGF-23 has significantly expanded into its present role as a key player in chronic kidney disease–mineral and bone disorder (CKD–MBD). From a clinical perspective, associations between circulating FGF-23, cardiovascular risk factors and mortality should be recognized. Although causal relationships between excess FGF-23 and adverse outcomes remain to be proven, this review attempts to identify potential mechanisms that presumably link FGF-23 to an increased cardiovascular risk.

The role of FGF-23 in CKD-MBD and cardiovascular disease: friend or foe?