Abstract
Like many novel discoveries, the recognition of a clinically relevant role of fibroblast growth factor 23 (FGF23) in nephrology was welcomed with almost untamed enthusiasm. Indeed, initial findings were stunning on several levels. First, the rise of circulating FGF23, as chronic kidney disease (CKD) progresses, is exponential, reaching values up to 1000-fold higher for patients with end-stage kidney disease than for healthy controls. Second, etiology-based analyses of observational data from many independent cohorts of patients with varying degrees of severity of kidney failure consistently revealed an unprecedented effect size of the associations of FGF23 with clinical end points.
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