Oral iron for anaemia in non-dialysis chronic kidney disease. The relationship between hepcidin-25, iron metabolism and inflammation

Background: Hepcidin and inflammatory markers can differentiate patients with chronic kidney disease who respond to oral iron therapy. Objectives: To assess if the answer to iron oral therapy is influenced by hepcidin or by inflammation and to describe the relationship between hepcidin, inflammation and anaemia in patients with non-dialysis chronic kidney disease. Methods: Non-randomized prospective study on a population of non-dialysis chronic kidney disease and anaemia attending a tertiary care hospital. Eligible patients were over 18 years, with no treatment for anaemia and estimated Glomerular Filtration Rate (eGFR)<60 ml/min/1.73 mp at least 6 months before enrolment. Exclusion criteria: bleeding, malignancy, infection, systemic or hepatic disease, immunosuppression, MCV higher than 100 fl, dialysis and renal transplantation. All patients received a four-week treatment with oral iron (Ferrous sulfate) at a dose of 105 mg once daily. Iron metabolism parameters, serum hepcidin-25, IL-6, TNF-α, Erythropoietin (EPO), high-sensitivity CRP were measured at baseline and after four weeks of oral iron therapy. Results: Four weeks of oral iron therapy significantly improved haemoglobin values (p<0.05). Serum hepcidin values were significantly higher after four weeks of oral iron compared with baseline. Hepcidin-25 was positively correlated with ferritin, serum iron, TSAT and TNF-alpha. A negative correlation between hepcidin-25, eGFR and serum EPO was demonstrated. In multivariate regression analysis, TNF-α was the parameter that best predicted hepcidin values. Conclusion: Our results agree that oral iron treatment is effective in raising haemoglobin in non-dialysis CKD patients after four weeks of treatment. Hepcidin seems to be more sensitive than ferritin to confirm the improvement in iron utilization. TNF-α was the best predictor of hepcidin values in our patients.