Hepcidin clearance is associated with erythropoietin requirement in stable hemodialysis patients .

Abstract

The discovery of hepcidin, the hormone regulating iron absorption and transport, has improved the understanding of anemia and erythropoietin treatment. Excessive hepcidin signaling causes anemia in chronic inflammatory conditions by restricting iron delivery to the bone marrow. Hepcidin is normally eliminated in the urine, and the high levels seen in renal failure are thought to contribute to renal anemia and resistance to erythropoietin. Clearance of hepcidin by hemodialysis was investigated in this study by measurement of plasma hepcidin before and after a single dialysis session in 204 patients. <u>Results:</u> Dialysis significantly reduced circulating hepcidin (p<0.001) with median (IQR) clearance 47.7 (34.2-61.0)%. Dialytic hepcidin clearance was correlated with spKt/V (R=0.202, p=0.006), but not related to session length or membrane flux. There was also a strong correlation between hepcidin clearance and erythropoietin dose (R=-0.193, p=0.007), sufficient to displace more traditional markers of erythropoietin resistance in a linear regression model, suggesting that increased dialytic removal of hepcidin could improve erythropoietin sensitivity. Hemodialysis reduces circulating hepcidin. Greater hepcidin clearance, which is related to spKt/V, is strongly associated with reduced erythropoietin requirement. This further implicates hepcidin in the pathogenesis of renal anemia and suggests that hepcidin could be a useful therapeutic target for dialysis patients. .