Purpose of review: To present emerging data on the role of fibroblast growth factor 23 (FGF23) in mineral metabolism and adverse outcomes in chronic kidney disease (CKD).
Recent findings: FGF23 regulates phosphorus and vitamin D metabolism. Its levels increase progressively beginning in early CKD, presumably as a physiological adaptation to maintain normal serum phosphate levels or normal phosphorus balance. FGF23 promotes phosphaturia and decreases production of calcitriol. Recent studies suggest that increased FGF23 is associated with mortality, left ventricular hypertrophy, endothelial dysfunction and progression of CKD. These results were consistently independent of serum phosphate levels.
Summary: FGF23 is emerging as a novel and exciting biomarker that may help identify which CKD patients might benefit most from aggressive management of disordered phosphorus metabolism. Future studies should determine whether increased FGF23 levels exert direct end-organ toxicity, such as in the heart, vessels and kidneys.