Division of Kidney and Dialysis, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan; Department of Kidney and Dialysis, Meiwa Hospital, Nishinomiya, Hyogo, Japan.
Division of Kidney and Dialysis, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
J Ren Nutr. 2018 Jul;28(4):270-277. doi: 10.1053/j.jrn.2017.12.009. Epub 2018 Apr 24.
Iron administration affects serum levels of intact (I-) fibroblast growth factor-23 (FGF23) and its cleavage product C-terminal (C-) FGF23 in iron-deficient patients on maintenance hemodialysis (MHD). The objective of this study was to compare the effect of oral or intravenous iron administration on serum levels of I-FGF23 and C-FGF23 in iron-deficient patients on MHD.
A prospective randomized study.
Participants on MHD with severe iron deficiency (n = 61).
Participants were randomized to receive oral iron (50 mg of sodium ferrous citrate daily; oral group, n = 29) or intravenous iron (40 mg of saccharated ferric oxide weekly; IV group, n = 32).
Changes in I-FGF23 and C-FGF23 after 10 weeks of treatment.
Iron supplementation significantly increased hemoglobin, mean corpuscular volume, ferritin, and transferrin saturation rate, and decreased erythropoiesis-stimulating agent dose and erythropoiesis-stimulating agent resistance index value. Serum phosphate, calcium, and intact parathyroid hormone levels did not change significantly during the study. I-FGF23 levels increased significantly in the IV group and did not change in the oral group, whereas C-FGF23 levels were significantly reduced in both groups. Serum interleukin-6 and tumor necrosis factor-α levels were increased in both groups. Multiple regression analysis indicated the relationship between iron or erythropoiesis and FGF23 metabolism.
Iron administration to patients on MHD with severe iron deficiency decreased C-FGF23 levels, whereas intravenous iron increased I-FGF23 levels though oral iron did not. If the target of chronic kidney disease-mineral and bone disorder therapy is reducing I-FGF23 levels, we suggest the use of oral iron.
铁剂治疗会影响维持性血液透析(MHD)患者血清中完整(I-)成纤维细胞生长因子 23(FGF23)及其裂解产物 C 端(C-)FGF23 的水平。本研究旨在比较口服和静脉补铁对 MHD 合并缺铁患者血清 I-FGF23 和 C-FGF23 水平的影响。
前瞻性随机研究。
MHD 伴严重缺铁患者(n=61)。
患者被随机分为口服补铁(每日 50mg 枸橼酸亚铁钠;口服组,n=29)或静脉补铁(每周 40mg 蔗糖铁;静脉组,n=32)。
治疗 10 周后 I-FGF23 和 C-FGF23 的变化。
补铁可显著增加血红蛋白、平均红细胞体积、铁蛋白和转铁蛋白饱和度,降低促红细胞生成素剂量和促红细胞生成素抵抗指数。研究期间,血清磷、钙和完整甲状旁腺激素水平无显著变化。静脉组 I-FGF23 水平显著升高,口服组无变化,而两组 C-FGF23 水平均显著降低。两组血清白细胞介素-6 和肿瘤坏死因子-α水平均升高。多元回归分析表明铁或促红细胞生成素与 FGF23 代谢之间的关系。
MHD 合并严重缺铁患者补铁可降低 C-FGF23 水平,而静脉补铁虽可增加 I-FGF23 水平,但口服铁剂却不能。如果慢性肾脏病-矿物质和骨异常治疗的目标是降低 I-FGF23 水平,我们建议使用口服铁剂。