Fibroblast growth factor 23 and hypophosphatemia: A case of hypophosphatemia along the rickets-osteomalacia spectrum

2Citations
Citations of this article
27Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Phosphorus is a key component of bone, and a deficiency results in poor mineralization along with other systemic symptoms of hypophosphatemia. Various causes of hypophosphatemia with renal wasting of phosphorus have been identified. These include the Fanconi syndrome, various genetic mutations of fibroblast growth factor 23 (FGF23) handling and the sodium/phosphate cotransporter, and those due to FGF23 secretion by mesenchymal tumors. Depending on the cause, vitamin D metabolism may also be impaired, which may amplify the deficiency in phosphorus and render treatment more challenging. Here, we report a case of hypophosphatemia and multiple stress fractures in a 20-year-old male college student living with chronic bone pain and anxiety about suffering further fractures. We further review the literature regarding this spectrum.

Cite

CITATION STYLE

APA

Georges, G. T., Nájera, O., Sowers, K., & Sowers, J. R. (2016, November 1). Fibroblast growth factor 23 and hypophosphatemia: A case of hypophosphatemia along the rickets-osteomalacia spectrum. CardioRenal Medicine. S. Karger AG. https://doi.org/10.1159/000449476

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free