Oral iron supplementation with sodium ferrous citrate reduces the serum intact and c-terminal FGF23 levels of maintenance hemodialysis patients

Background/Aim Iron deficiency stimulates fibroblast growth factor 23 (FGF23) transcription. This study aimed to determine whether oral ferrous iron (Fe2+) reduces the serum FGF23 levels of iron-deficient maintenance hemodialysis (MHD) patients in the same way as oral ferric iron (Fe3+). Methods Thirty-one MHD patients with iron deficiency were enrolled in this prospective study. Patients who had taken iron supplements during the 8 weeks before the study were excluded. The patients’ iron stores and their serum FGF23, phosphate, intact parathyroid hormone (iPTH), albumin, C-reactive protein (CRP), and albumin-adjusted calcium (Ca) levels were examined at the baseline and after 3 months’ treatment with sodium ferrous citrate (Fe2+). Results The patients’ transferrin saturation values and serum iron and ferritin levels were significantly increased after 3 months’ treatment (P < 0.01), as were their serum albumin levels (P < 0.05). Conversely, their serum intact FGF23 (iFGF23) [1820 (342-4370) vs. 1240 (214-2940) pg/ml, P < 0.05], C-terminal FGF23 (cFGF23) [309 (120-1211) vs. 259 (99-600) pg/ml, P < 0.05)], and CRP levels (P < 0.01) were significantly reduced after 3 months’ treatment. No changes were detected in the patients’ serum iFGF23:cFGF23 ratios or their serum phosphate, Ca, or iPTH levels. The changes in the patients’ serum iFGF23 and cFGF23 levels induced by sodium ferrous citrate supplementation were shown to be attributable to changes in their serum ferritin levels (P < 0.05). Conclusion Short-term oral iron supplementation with sodium ferrous citrate replenished the iron stores and reduced the serum iFGF23 and cFGF23 levels of MHD patients with iron deficiency without affecting their serum phosphate, Ca, or iPTH levels.