Show Summary Details
Page of

FGF23 in renal failure 

FGF23 in renal failure
FGF23 in renal failure

Katherine Wesseling-Perry

and Myles Wolf

Page of

PRINTED FROM OXFORD MEDICINE ONLINE ( © Oxford University Press, 2020. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

date: 10 August 2020

FGF23 plays a central role in phosphorus metabolism. This role was initially delineated by the study of genetic and acquired conditions of hypophosphatemic rickets but the greatest clinical impact of the discovery of FGF23 may be in the management of CKD patients. In patients with CKD, FGF23 levels rise as renal function declines, likely due to decreasing capacity of the damaged kidney to excrete dietary phosphorus loads. Rising FGF23 levels appear to contribute to the initiation of secondary hyperparathyroidism in CKD patients; however, increased levels of FGF23 also appear to contribute to or serve as markers of accelerated progression to renal failure, increased rates of mortality, and alterations in skeletal mineralization. Collectively, these results suggest that the effects of FGF23 on end-organ function in the context of chronic kidney disease differ markedly from the physiology observed in individuals with normal renal function.

Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.

Please subscribe or login to access full text content.

If you have purchased a print title that contains an access token, please see the token for information about how to register your code.

For questions on access or troubleshooting, please check our FAQs, and if you can't find the answer there, please contact us.