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JBMR Plus. 2020 Dec 09;5(2):e10437. doi: 10.1002/jbm4.10437. eCollection 2021 Feb.

Renal Phosphate Handling: Independent Effects of Circulating FGF23, PTH, and Calcium.

JBMR plus

Malachi J McKenna, Rachel K Crowley, Patrick J Twomey, Mark T Kilbane

Affiliations

  1. UCD School of Medicine University College Dublin Dublin Ireland.
  2. Department of Clinical Chemistry St. Vincent's University Hospital Dublin Ireland.
  3. Department of Endocrinology St. Vincent's University Hospital Dublin Ireland.

PMID: 33615106 PMCID: PMC7872336 DOI: 10.1002/jbm4.10437

Abstract

Excess fibroblast growth factor 23 (FGF23), excess PTH, and an increase in extracellular calcium cause hypophosphatemia by lowering the maximum renal phosphate reabsorption threshold (TmP/GFR). We recently reported two cases of X-linked hypophosphatemia (XLH) with severe tertiary hyperparathyroidism who had normalization of TmP/GFR upon being rendered hypoparathyroid following total parathyroidectomy, despite marked excess in both C-terminal FGF23 (cFGF23) and intact FGF23 (iFGF23). We explored the effects of FGF23, PTH, and calcium on TmP/GFR in a cross-sectional study (

© 2020 The Authors. JBMR Plus published by Wiley Periodicals LLC. on behalf of American Society for Bone and Mineral Research.

Keywords: FIBROBLAST GROWTH FACTOR 23; HYPERPARATHYROIDISM; HYPOPARATHYROIDISM; PARATHYROID HORMONE; X‐LINKED HYPOPHOSPHATEMIA

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