Hepcidin Predicts Hemoglobin Response to Iron Loading
Damien Ashby, MD
SAN DIEGO—Plasma hepcidin may be a more useful guide to anemia management in hemodialysis (HD) patients than traditional iron parameters, British investigators reported here at the American Society of Nephrology's Renal Week conference.
They found that plasma hepcidin levels predict hemoglobin (Hb) response to IV iron loading and may reflect adequate iron availability or relative erythropoietin deficiency.
A hormone made in the liver, hepcidin inhibits iron absorption and recycling.
Damien Ashby, MD, of the Imperial College Kidney and Transplant Institute, Hammersmith Hospital, London, and colleagues measured plasma hepcidin levels in 67 stable HD patients before IV iron loading, which was indicated by ß levels of ferritin (below 400 ng/mL) or iron (less than 10 nmol/mL). Patients then received 200 mg iron sucrose IV at each of the next five HD sessions, with Hb response assessed the following month.
Of the 67 subjects, 43 (64%) were responders, defined as patients whose Hb increased after iron loading. Plasma hepcidin levels at baseline were significantly higher in subsequent nonresponders than in responders, the study showed. No other measured parameter was related to subsequent Hb response, including ferritin, iron, erythropoietin dose, C-reactive protein, and albumin.
In a separate study of six healthy individuals, the same research team found that erythropoietin administration is associated with a profound reduction in circulating hepcidin. In the study, Dr. Ashby's group measured plasma iron parameters at multiple timepoints before and after a single injection of erythropoietin and measured hepcidin with a recently developed radioimmunoassay.
In all subjects, erythropoietin injection was followed by a marked reduction in circulating hepcidin lasting more than 14 days; erythropoietin levels returned to baseline by seven days.
In addition, levels of circulating iron and ferritin drifted down during the week, but these changes occurred after the reduction in hepcidin. “The reduction in hepcidin therefore prevents circulating iron depletion when demand is expected to increase,” the authors wrote in a poster.