FGF23 AND ALTERED MINERAL HOMEOSTASIS IN KIDNEY DISEASE AND FOLLOWING INTRAVENOUS IRON.

Abstract

Fibroblast growth factor 23 (FGF23) is an endocrine hormone that stimulates renal phosphate excretion and suppresses circulating concentrations of 1,25-dihydroxyvitamin D (1,25D). These effects of FGF23 are most evident in rare diseases that are characterized by FGF23-mediated hypophosphatemic rickets-osteomalacia. More commonly, elevated FGF23 is a ubiquitous, early consequence of chronic kidney disease (CKD) in which it helps to maintain normal serum phosphate levels but causes secondary hyperparathyroidism by suppressing 1,25D, and directly promotes cardiovascular disease and death. Elevated FGF23 is also a common complication of intravenous administration of ferric carboxymaltose (FCM), which is widely used to treat iron deficiency anemia. Among patients with normal kidney function who receive FCM, the resulting increase in FGF23 and subsequent FGF23-mediated reduction of 1,25D and secondary hyperparathyroidism promote hypophosphatemia that can be symptomatic, severe, and associated with musculoskeletal complications. Ongoing research is needed to design novel therapeutic approaches to mitigate FGF23-related illnesses.