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FGF23 Elevation and Hypophosphatemia after Intravenous Iron Polymaltose: A Prospective Study

Department of Endocrinology (B.J.S., P.J.H., J.H.L., S.G.S.), Christchurch Hospital, Christchurch 8011, New Zealand; and Department of Medicine (C.M.F.), Christchurch School of Medicine and Health Sciences, Christchurch 8011, New Zealand

Address all correspondence and requests for reprints to: Dr. Belinda Schouten, Department of Endocrinology, Christchurch Hospital, Christchurch, New Zealand. E-mail: Belinda.Robb{at}cdhb.govt.nz.

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 <0.05) and 1,25(OH)₂D (R = –0.71; P < 0.05).

Conclusion: Parenteral iron suppresses renal tubular phosphate reabsorption and 1-hydroxylation of vitamin D resulting in hypophosphatemia. Our data suggest that this is mediated by an increase in FGF23.