Abstract
Purpose of reviewHyperphosphatemia, 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 findingsNew 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.SummaryNew 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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 359-366 |
| Number of pages | 8 |
| Journal | Current opinion in nephrology and hypertension |
| Volume | 29 |
| Issue number | 4 |
| DOIs | |
| State | Published - Jul 1 2020 |
Funding
This study was supported by the American Heart Association grant 19POST34380583 to G.C. and by grants from the National Institute of Health (R01DK102815, R01DK114158) to V.D. V.D. received research funding from Akebia and has received research funding from Vifor Pharma and consulting honoraria from Keryx Biopharmaceuticals, Vifor Pharma, Luitpold, and Amgen. All other authors have nothing to disclose.
Keywords
- anemia
- cardiovascular disease
- chronic kidney disease
- iron
- phosphate
ASJC Scopus subject areas
- Nephrology
- Internal Medicine
