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J Am Soc Nephrol. 2010 Sep;21(9):1427-35. doi: 10.1681/ASN.2009121293. Epub 2010 May 27.

Forging forward with 10 burning questions on FGF23 in kidney disease.

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  • 1Division of Nephrology and Hypertension, University of Miami Miller School of Medicine, 1120 NW 14th Street, CRB, C-221, Room 819, Miami, FL 33136, USA.


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 per-nephron 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.

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