同时管理紊乱的磷酸盐和铁稳态，以纠正慢性肾脏病中的成纤维细胞生长因子 23 及其相关结局。
Simultaneous management of disordered phosphate and iron homeostasis to correct fibroblast growth factor 23 and associated outcomes in chronic kidney disease.
机构信息
Division of Nephrology and Hypertension, Department of Medicine, and Center for Translational Metabolism and Health, Institute for Public Health and Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
出版信息
Curr Opin Nephrol Hypertens. 2020 Jul;29(4):359-366. doi: 10.1097/MNH.0000000000000614.
PURPOSE OF REVIEW
Hyperphosphatemia, iron deficiency, and anemia are powerful stimuli of fibroblast growth factor 23 (FGF23) production and are highly prevalent complications of chronic kidney disease (CKD). In this manuscript, we put in perspective the newest insights on FGF23 regulation by iron and phosphate and their effects on CKD progression and associated outcomes. We especially focus on new studies aiming to reduce FGF23 levels, and we present new data that suggest major benefits of combined corrections of iron, phosphate, and FGF23 in CKD.
RECENT FINDINGS
New studies show that simultaneously correcting iron deficiency and hyperphosphatemia in CKD reduces the magnitude of FGF23 increase. Promising therapies using iron-based phosphate binders in CKD might mitigate cardiac and renal injury and improve survival.
SUMMARY
New strategies to lower FGF23 have emerged, and we discuss their benefits and risks in the context of CKD. Novel clinical and preclinical studies highlight the effects of phosphate restriction and iron repletion on FGF23 regulation.
目的综述
高磷血症、缺铁和贫血是成纤维细胞生长因子 23（FGF23）产生的强大刺激因素，也是慢性肾脏病（CKD）的高发并发症。在本文中，我们从新的角度探讨了铁和磷对 FGF23 的调节及其对 CKD 进展和相关结局的影响。我们特别关注旨在降低 FGF23 水平的新研究，并提出新的数据表明联合纠正铁、磷和 FGF23 在 CKD 中的重要益处。
最近的发现
新的研究表明，同时纠正 CKD 中的缺铁和高磷血症可降低 FGF23 增加的幅度。在 CKD 中使用铁基磷结合剂的有前途的治疗方法可能减轻心脏和肾脏损伤并提高生存率。
总结
已经出现了降低 FGF23 的新策略，我们在 CKD 的背景下讨论了它们的益处和风险。新的临床和临床前研究强调了限制磷酸盐和补充铁对 FGF23 调节的影响。
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