Serum hepcidin-25 and response to intravenous iron in patients with non-dialysis chronic kidney disease

Abstract

Hepcidin-25 is an iron regulator which reduces iron absorption and promotes sequestration in the reticulo-endothelial system. We investigated hepcidin and traditional iron storage marker utility in predicting haemoglobin increment following bolus intravenous iron. The cohort included 129 consecutive non-dialysis chronic kidney disease patients that attended for intravenous iron over a 6-month period. Serum hepcidin-25 levels (determined by mass spectrometry) pre iron infusion and 6 weeks post were compared with ferritin and transferrin saturation in multivariate models. Log10 ferritin [coefficient 0.559 (0.435-0.684) p < 0.001] and log10 high-sensitive C-reactive protein [coefficient 0.092 (0.000-0.184) p = 0.049] were significantly associated with baseline log10 hepcidin-25 levels. Log10 estimated glomerular filtration rate was the only independent determinant of pre-infusion haemoglobin [coefficient 1.37 (0.16-2.59) p = 0.027]. Log10 hepcidin-25 was an independent predictor of haemoglobin increment 6 weeks following iron infusion [coefficient -0.84 (-1.38 to -0.31) p = 0.002]. Ferritin, transferrin saturation and hepcidin had similar predictive utility for a 1 g/dl haemoglobin increase (c-statistics: 0.68, 0.70, 0.69). Hepcidin is an iron sensor marker which predicts the magnitude of haemoglobin increment following protocolised intravenous iron infusion. Although displaying similar predictive performance to ferritin and transferrin saturation, hepcidin may also play a mechanistic role.