Fibroblast growth factor-23 and cardiac structure and function.

Fibroblast growth factor-23 (fgf-23) is a phosphaturic factor previously associated with left ventricular hypertrophy and systolic dysfunction among individuals with chronic kidney disease. whether fgf-23 acts directly to induce left ventricular hypertrophy,potentially independent of its klotho coreceptor,remains uncertain. we investigated associations of fgf-23 with cardiac structural abnormalities among individuals with a broad range of kidney function and explored potential biological mechanisms using cardiac magnetic resonance imaging and histology in klotho-null mice,an established model of constitutively elevated fgf-23. among 887 participants with coronary artery disease in the heart and soul study,fgf-23 was modestly associated with worse left ventricular ejection fraction (-1.0% per standard deviation increase in lnfgf-23; standard error,0.4%),but was not associated with the overall prevalence of concentric hypertrophy (odds ratio,1.5; ci,0.9 to 2.4) or eccentric hypertrophy (odds ratio,1.1; ci,0.9 to 1.3). fgf-23 was only associated with concentric hypertrophy among individuals with diminished kidney function (egfr <60 ml/min per 1.73 m(2); odds ratio,2.3; ci,1.0 to 5.3; p-interaction=0.28). comparing klotho-null with wild-type mice,null mice did not have greater left ventricular mass (p=0.37) or a lower ejection fraction (p=0.94). together,our results suggest that fgf-23 is unlikely to have major effects on cardiovascular structure and function among patients free of substantial chronic kidney disease,and these effects may not be independent of the klotho coreceptor.