Fibroblast growth factor 23 and bone mineralisation

Abstract

A hormone secreted by bone-forming cells may play a critical role in the bone disorders in kidney disease. In their review Quan Yan, from the West China Hospital of Stomatology in Chengdu, and colleagues noted that levels of fibroblast growth factor 23 (FGF-23) increase with a decline in kidney function. Elevated levels have been linked to end-stage renal disease, cardiovascular disease and death. The mechanisms underlying this association with poor outcomes could be explained by the hormone’s ability to increase inflammation. FGF-23 is also thought to play a critical role in mineral ion disorders and bone metabolism in these patients. The authors suggest studying whether deactivating FGF-23 in kidney disease would halt bone damage without having other adverse effects on the body.

Keywords

bone mineralisation / chronic kidney disease / fibroblast growth factor 23

References

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