Open AccessFibroblast Growth Factor–23 and Cardiac Structure and Function
Author(s) -
Agarwal Isha,
Ide Noriko,
Ix Joachim H.,
Kestenbaum Bryan,
Lanske Beate,
Schiller Nelson B.,
Whooley Mary A.,
Mukamal Kenneth J.
Publication year - 2014
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.113.000584
Subject(s) - medicine , ejection fraction , cardiology , kidney disease , odds ratio , fibroblast growth factor 23 , muscle hypertrophy , left ventricular hypertrophy , concentric hypertrophy , risk factor , coronary artery disease , endocrinology , fibroblast growth factor , renal function , heart failure , blood pressure , parathyroid hormone , receptor , calcium
Background 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. Methods and Results Among 887 participants with coronary artery disease in the H eart and S oul S tudy, FGF ‐23 was modestly associated with worse left ventricular ejection fraction (−1.0% per standard deviation increase in ln FGF ‐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). Conclusions 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.