Anemia in heart and kidney allograft recipients: is there a role for hepcidin?

The production by hepatocytes of hepcidin, a small defensin-like peptide, is modulated in response to anemia, hypoxia, or inflammation. We studied hepcidin as a marker of iron status (serum iron, ferritin, and soluble receptor of transferrin [sTfR], and as a marker of inflammation among 170 prevalent kidney transplantation (KT) patients and 168 prevalent orthotopic heart transplant (OHT) patients. In addition, we assessed the prevalence of anemia and its relation to measurements of hepcidin, sTfR, and high-sensitivity C-reactive protein, using commercially available enzyme-linked immunosorbent assay (ELISA) kits. Prevalence of anemia was 37% in KT patients and 34% in OHT patients according to the World Health Organisation (WHO) definition. Anemic KT patients displayed significantly higher values of serum creatinine, hepcidin, hsCRP, ferritin, and proteinuria associated with greater use of mTOR and significantly lower CSA therapy. The hemoglobin and estimated glomerular filtration rate (eGFR). Upon multiple regression analysis eGFR, ferritin, and hsCRP independently predicted hepcidin levels, explaining 78% of the variation in hepcidin. Anemic OHT patients showed significantly lower GFR, red blood cell (RBC), and hemoglobin values and significantly higher creatinine and NT-proBNP content. Upon multiple regression analysis the predictors of serum hepcidin were eGFR and ferritin, which explained 68% of the variation in hepcidin. The prevalence of anemia is relatively high and not adequately treated (mainly due to reimbursement regulations) among heart and kidney allograft recipients. In conclusion, elevated hepcidin levels in heart and kidney transplant recipients suggest subclinical inflammation and impaired kidney function.