Abstract: Iron transport disorder is a common cause of refractory anemia in chronic kidney disease (CKD) patients. Hepcidin is a key hormone for the body to maintain iron homeostasis, and it can regulate iron metabolism into the negative direction. This feedback regulation process is regulated by multiple pathways, including bone morphogenetic protein (BMP)/ Smad signaling pathway, Janus kinase (JAK) /signal transducer and activator of transcription 3 (STAT3) pathway, inflammation, erythropoiesis, hypoxia, etc. Hepcidin is the main target for the treatment of iron metabolism imbalance in clinical practice. In recent years, a variety of hepcidin regulation-related drugs have appeared oriented and abroad. Among them, hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHI） drugs such as Roxadustat are believed to effectively reduce the expression of hepcidin, increase serum iron levels, promote iron utilization, and promote red blood cell production to treat anemia in CKD patients.

Key words: hepcidin, iron metabolism, hypoxia-inducible factor prolyl hydroxylase inhibitors, Roxadustat