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Published on: May 10, 2022
FGF23 elevation and hypophosphatemia after intravenous iron polymaltose: a prospective study
Belinda J Schouten1, Penelope J Hunt, John H Livesey
1Department of Endocrinology, Christchurch Hospital, Christchurch, New Zealand. Belinda.Robb@cdhb.govt.nz
The Journal of Clinical Endocrinology and Metabolism
|April 16, 2009
Summary
Parenteral iron administration causes hypophosphatemia by suppressing phosphate reabsorption and vitamin D activation. This effect appears to be mediated by increased fibroblast growth factor 23 (FGF23) levels.
Area of Science:
- Endocrinology
- Nephrology
- Mineral Metabolism
Background:
- Parenteral iron is linked to hypophosphatemia.
- Fibroblast growth factor 23 (FGF23) regulates phosphate homeostasis.
- Previous findings suggest a link between iron, FGF23, and hypophosphatemia.
Purpose of the Study:
- To prospectively investigate the impact of parenteral iron polymaltose on phosphate homeostasis.
- To determine if changes in phosphate homeostasis are related to FGF23 alterations.
Main Methods:
- Eight outpatients received intravenous iron polymaltose.
- Measurements included plasma phosphate, 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)(2)D], PTH, FGF23, and urinary phosphate reabsorption.
- Data were collected at baseline and weekly for at least 3 weeks.
Main Results:
- Plasma phosphate and tubular reabsorption of phosphate significantly decreased post-iron administration.
- 1,25(OH)(2)D levels dropped significantly, while 25(OH)D levels remained unchanged.
- FGF23 levels markedly increased, correlating with decreased serum phosphate and 1,25(OH)(2)D.
Conclusions:
- Parenteral iron impairs renal phosphate reabsorption and vitamin D activation, leading to hypophosphatemia.
- Increased FGF23 levels appear to mediate these effects.
- This study elucidates the mechanism of iron-induced hypophosphatemia.