Forging forward with 10 burning questions on FGF23 in kidney disease

Myles Wolf*

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

197 Scopus citations

Abstract

The discovery of fibroblast growth factor 23 (FGF23) as the causal factor in the pathogenesis of rare forms of hypophosphatemic rickets is rapidly reshaping our understanding of disordered mineral metabolism in chronic kidney disease (CKD). Excessive production of FGF23 by osteocytes is an appropriate compensation to help maintain normal phosphorus metabolism in these patients. Beginning in early CKD, progressive increases in levels of FGF23 enhance phosphaturia on a pernephron basis and inhibit calcitriol production, thereby contributing centrally to the predominant phosphorus phenotype of predialysis kidney disease: normal serum phosphate, increased fractional excretion of phosphate, and calcitriol deficiency. A proliferation of studies linking phosphorus and now FGF23 excess to adverse renal and cardiovascular outcomes in patients with CKD is setting the stage for novel clinical trials that could ultimately bring FGF23 testing into the clinic. Ten burning questions must be addressed to galvanize FGF23 research further in CKD.

Original languageEnglish (US)
Pages (from-to)1427-1435
Number of pages9
JournalJournal of the American Society of Nephrology
Volume21
Issue number9
DOIs
StatePublished - Sep 2010

ASJC Scopus subject areas

  • Nephrology

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