FGF23 Elevation and Hypophosphatemia after Intravenous Iron Polymaltose: A Prospective Study
Open Access
- 1 July 2009
- journal article
- research article
- Published by The Endocrine Society in Journal of Clinical Endocrinology & Metabolism
- Vol. 94 (7), 2332-2337
- https://doi.org/10.1210/jc.2008-2396
Abstract
Context: Parenteral iron administration has been associated with hypophosphatemia. Fibroblast growth factor 23 (FGF23) has a physiological role in phosphate homeostasis via suppression of 25-hydroxyvitamin D [25(OH)D] activation and promotion of phosphaturia. We recently reported a case of iron-induced hypophosphatemic osteomalacia associated with marked FGF23 elevation. Objective: Our objective was to prospectively investigate the effect of parenteral iron polymaltose on phosphate homeostasis and to determine whether any observed change was related to alterations in circulating FGF23. Design, Setting, and Participants: Eight medical outpatients prescribed iv iron polymaltose were recruited. Plasma phosphate, 25(OH)D, 1,25-dihydroxyvitamin D [1,25(OH)2D], PTH, FGF23, and urinary tubular reabsorption of phosphate were measured prior to iron administration and then weekly for a minimum of 3 wk. Results: Plasma phosphate fell from 3.4 ± 0.6 mg/dl at baseline to 1.8 ± 0.6 mg/dl at wk 1 (P < 0.0001) associated with a fall in percentage tubular reabsorption of phosphate (90 ± 4.8 to 68 ± 13; P < 0.001) and 1,25(OH)2D (54 ± 25 to 9 ± 8 pg/ml; P < 0.001). These indices remained significantly suppressed at wk 2 and 3. 25(OH)D levels were unchanged. FGF23 increased significantly from 43.5 pg/ml at baseline to 177 pg/ml at wk 1 (P < 0.001) with levels correlating with both serum phosphate (R = −0.74; P 2D (R = −0.71; P < 0.05). Conclusion: Parenteral iron suppresses renal tubular phosphate reabsorption and 1α-hydroxylation of vitamin D resulting in hypophosphatemia. Our data suggest that this is mediated by an increase in FGF23.Keywords
This publication has 37 references indexed in Scilit:
- Iron polymaltose-induced FGF23 elevation complicated by hypophosphataemic osteomalaciaAnnals of Clinical Biochemistry: International Journal of Laboratory Medicine, 2009
- Genetic Evidence of Serum Phosphate-Independent Functions of FGF-23 on BonePLoS Genetics, 2008
- Overexpression of Fibroblast Growth Factor 23 Suppresses Osteoblast Differentiation and Matrix Mineralization In VitroJournal of Bone and Mineral Research, 2008
- The emerging role of the fibroblast growth factor-23–klotho axis in renal regulation of phosphate homeostasisJournal of Endocrinology, 2007
- Clinical update: intravenous iron for anaemiaThe Lancet, 2007
- FGF23 Concentrations Vary With Disease Status in Autosomal Dominant Hypophosphatemic RicketsJournal of Bone and Mineral Research, 2007
- Fibroblast Growth Factor-23 Is Regulated by 1α,25-Dihydroxyvitamin DJournal of Bone and Mineral Research, 2005
- Hepcidin—a regulator of intestinal iron absorption and iron recycling by macrophagesBest Practice & Research Clinical Haematology, 2005
- Fibroblast Growth Factor 23 in Oncogenic Osteomalacia and X-Linked HypophosphatemiaThe New England Journal of Medicine, 2003
- Saccharated Ferric Oxide-Induced Osteomalacia in Japan: Iron-Induced Osteopathy Due to Nephropathy.Endocrine Journal, 1998