Abstract
Mutations and overexpression of the hormone fibroblast growth factor 23 (FGF23) were discovered 20 years ago as the cause of autosomal dominant hypophosphatemic rickets and tumor-induced osteomalacia, respectively. Subsequently, numerous studies first demonstrated the role of FGF23 in regulating phosphate and calcium homeostasis and second its involvement in inflammation, iron metabolism, and erythropoiesis.1 Moreover, a steadily increasing number of observational studies in patients with advanced stages of chronic kidney disease (CKD) showed associations of increased circulating FGF23 levels with intermediate and hard outcomes, including myocardial hypertrophy and dysfunction, cardiovascular events, and mortality.
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