A Possible Role of Hepcidin in the Pathogenesis of Anemia in Heart Allograft Recipients

Abstract

Hepcidin, a small defensin-like peptide produced by hepatocytes, is modulated in response to anemia, hypoxia, or inflammation. We studied hepcidin correlations with markers of iron status and of inflammation among 134 prevalent recipients of heart allografts (OHT). In addition, we assessed the prevalence of anemia and its relation to hepcidin. Soluble transferrin (sTfR), interleukin (IL)-6, cystatin C, and hepcidin receptors were measured using commercially available kits. According to the World Health Organization definition, the prevalence of anemia was 40%. Anemic OHT showed significantly higher values of serum creatinine, cystatin C, hepcidin, IL-6, ferritin, soluble transferrin receptor, NT-proBNP, everolimus treatment, and significantly lower quantities of cholesterol, low-density lipoprotein, ejection fraction, hemoglobin, erythrocyte count, and estimated glomerular filtration rate (GFR) (Modification of Diet in Renal Disease, CKD-EPI). Hepcidin correlated with total iron binding capacity, ferritin, IL-6, hemoglobin, erythrocyte count, cystatin C, NT-proBNP, creatinine, and GFR. Multiple regression analysis showed hepcidin to be independently related only to ferritin, explaining 76% of the variation in hepcidin. The prevalence of anemia is relatively great among the population of heart allograft recipients. In these patients the pathogenesis of anemia is multifactorial. Elevated hepcidin levels in heart transplant recipients may be due to low-grade inflammation, which is frequently encountered in this population, as well as probably to impaired renal function, but it does not seem to be a major pathogenic factor for anemia among this population.