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Clin Kidney J. 2012 Jun;5(3):240-3. doi: 10.1093/ckj/sfs031. Epub 2012 Mar 29.

Oncogenic osteomalacia illustrating the effect of fibroblast growth factor 23 on phosphate homeostasis.

Clinical kidney journal

Per-Anton Westerberg, Torbjörn Linde, Dirk Vanderschueren, Jaak Billen, Ivo Jans, Östen Ljunggren

Affiliations

  1. Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
  2. Laboratory of diagnostic medicine, Katholieke Universiteit Leuven, Leuven, Belgium ; laboratory of experimental medicine and endocrinology, Katholieke Universiteit Leuven, Leuven, Belgium.

PMID: 26069775 PMCID: PMC4400509 DOI: 10.1093/ckj/sfs031

Abstract

In oncogenic osteomalacia (OOM), fibroblast growth factor 23 (FGF23) induces renal phosphate wasting and inhibits the appropriate increase of calcitriol. A patient suffering from OOM is described. Serum calcium, phosphate, biointact parathyroid hormone and intact FGF23 as well as the calcitriol and 24,25-vitamin D levels were measured before and after tumour removal. The clinical approach to a patient with hypophosphataemia is discussed and the changes in mineral metabolism after removal of a FGF23-producing tumour are described.

Keywords: FGF23; mineral metabolism; osteomalacia; phosphate

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