P0860intravenous Iron Administration Suppresses Endogenous Erythropoietin Secretion in Patients With Chronic Kidney Disease

Abstract

Background and Aims Iron therapy may induce inflammatory response that may indirectly affect endogenous erythropoietin (EPO) production. We postulated that increased secretion of FGF-23 may provide a link between intravenous iron administration and suppression of endogenous EPO secretion. Evaluation of a short-term effect of intravenous iron sucrose administration on the secretion of endogenous EPO in patients with chronic kidney disease (CKD). Method 35 non-dialysed patients with G3b-5 CKD were included. All patients received 100 mg of intravenous iron infusion (iron (III)-hydroxide sucrose complex) daily for 5 days. Plasma concentration of EPO, iFGF-23, cFGF-23, PTH, bone alkaline phosphatase (BAP), phosphorus (PO4) and calcium (Ca) were measured before and two hours after the first and third iron infusion and at the end of iron therapy. Results EPO concentration at the end of iron treatment was significantly lower compared to 2 h after the first iron infusion (p<0.001) and before the third dose (p<0.001) (12.6 [31.2] mIU/mL, 30.9 [38.3] mIU/mL, 33.4 [41.3] mIU/mL and, respectively). Conversely, serum iFGF-23 increased significantly after the third dose (61.1 [401.5] pg/mL; p<0.05) and after the treatment (92.1 [849.7] pg/mL; p<0.01) compared to pre-treatment value (48.4 [403.8] pg/mL). cFGF-23 concentration decreased significantly after the first dose of iron (491.8 [828.6] vs. 339.2 [875.8] RU/mL; p<0.01) and after the completion of the therapy (398.7 [931.9]) vs. baseline (p<0.05). There was no linear correlation between EPO and FGF-23. Conclusion Intravenous iron therapy increases the secretion of FGF-23 and supresses endogenous EPO production but these two effects do not seem to be related.