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Increased hepcidin-25 and erythropoietin responsiveness in patients with cardio-renal anemia syndrome.
Future Cardiol. 2010 Nov;6(6):769-71
Authors: Kato A
Abstract
Hepcidin is a key regulator controlling iron intestinal absorption and distribution through the body. The article by van der Putten et al. examined the association between hepcidin-25 and erythropoietin responsiveness and inflammation in erythropoietin-naive, iron-replete patients with chronic heart failure and chronic kidney disease. A cross-sectional observation revealed that serum hepcidin-25 was elevated almost twofold when compared with levels in healthy subjects. Hepcidin-25 was inversely correlated with hemoglobin (r(2) = 0.18; p < 0.02), and positively with ferritin (r(2) = 0.51; p < 0.01) and transferrin saturation (r(2) = 0.14; p < 0.03), while it did not correlate with levels of IL-6 and highly sensitive C-reactive protein. They found that 2-week erythropoietin therapy (50 IU/kg/week) significantly decreased hepcidin-25 levels. The magnitude of the decrease in hepcidin-25 levels correlated with the increase in reticulocytes (r(2) = 0.23; p < 0.03) and soluble transferrin receptor (r(2) = 0.23; p = 0.03), but not with inflammatory markers. A decline in hepcidin-25 correlated with the increment of hemoglobin after 6 months (r(2) = 0.49; p < 0.01). The findings convincingly suggest that hepcidin-25 may be useful in predicting erythropoietin responsiveness in stable chronic heart failure patients. However, further studies will be needed to establish clinically available methods to reliably measure hepcidin-25 level.
PMID: 21142632 [PubMed - indexed for MEDLINE] Read more |
