Proposed mechanism of ferric carboxymaltose (FCM)-induced hypophosphatemia. Iron deficiency increases FGF23 production, but this is balanced by increased cleavage of FGF23 into its C- and N-terminal fragments that do not affect phosphate homeostasis. Through unclear mechanisms, FCM appears to reduce FGF23 cleavage, resulting in higher levels of full-length FGF23 and, thus, hypophosphatemia. Independent of phosphate homeostasis, C-terminal FGF23 peptides appear to share a negative feedback loop with hepcidin to regulate iron homeostasis by inhibiting bone morphogenic protein (BMP) 2/9-mediated hepcidin production.