Hypoxia-inducible factor prolyl hydroxylase inhibitor, C-terminal fibroblast growth factor 23 fragments, and hepcidin

With great interest, I read the impressive new findings by Hanudel et al. recently published in Kidney International showing that erythroferrone-mediated suppression of hepcidin is not essential for beneficial effects vadadustat, as hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI), on anemia chronic kidney disease.1 In discussion section, authors meticulously listed several alternative pathways may function predominant mechanism linking HIF-PHI and suppression.