Tumor-induced osteomalacia

Abstract

Tumor-induced osteomalacia (TIO) is an acquired disorder of isolated renal phosphate wasting associated with tumors, typically of mesenchymal origin. Patients with TIO share similar biochemical and skeletal phenotypes with patients who have autosomal dominant hypophosphatemic rickets (ADHR) and X-linked hypophosphatemia. The study of TIO introduced the idea of the existence of circulating factors, referred to as ‘phosphatonins’, produced by the tumor, which act upon the kidney to reduce phosphate reabsorption. Although several factors have been identified, the phosphatonin FGF-23, also identified as the causative factor in ADHR, is currently the best characterized of these factors relative to phosphate handling. This review describes the importance of TIO in understanding phosphate homeostasis in the context of new endocrine interactions between the skeleton and the kidney.

Keywords::

• FGF-23
• fibroblast growth factor-23
• FRP4
• hypophosphatemia
• MEPE
• oncogenic osteomalacia

Acknowledgements

We acknowledge the editorial and scientific contributions of Lelia Summers.

Financial & competing interests disclosure

Kenneth E White receives royalties for licensing the FGF-23 gene to Kyowa Hakko Kirin, Ltd. The authors would like to acknowledge support by NIH grant DK063934 (Kenneth E White), the Showalter Foundation, and the Indiana Genomics Initiative (INGEN) of Indiana University, supported in part by the Lilly Endowment, Inc. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.