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Background  Fibroblast Growth Factor (FGF) 23 influences endothelial integrity and few reports have studied the association between FGF23 and Kawasaki syndrome (KS), a childhood vasculitis displaying a high risk of subsequent cardiac abnormalities (CaA).    Aim  To investigate the genetic variation in the  FGF23  gene in a cohort of KS children and its association with serum FGF23 levels and eventual development of CaA, including both coronary artery dilatations and aneurysms.    Patients and methods  84 Italian KS children were recruited; 24/84 (28.6%) developed CaA. Each patient underwent evaluation of serum FGF23 levels and  FGF23  genotype: the frequency of the c.212-37insC (rs3832879) polymorphism in intron 1 was examined and compared with sex, age at disease onset, fever duration, laboratory data, and occurrence of CaA. Univariate statistical analysis of categorical parameters was performed by the Pearson’s Chi-square test or Fisher’s exact test as appropriate. Parametric variables were assessed by Student’s t-test for unpaired data. Independent predictors of disease were studied by a logistic regression model.    Results  28/84 patients carried the  FGF23  polymorphism (33.3%) and had higher serum FGF23 levels ( p  < 0.01).  FGF23  polymorphism was significantly associated with CaA compared to wild type  FGF23  children (respectively,  p  = 0.03 and  p  = 0.05). The comparison with demographical, clinical or laboratory data was not significant.    Conclusions  The prevalent segregation of the c.212-37insC polymorphism in children with CaA advocates a possible functional  FGF23  role in the predisposition to higher serum levels of FGF23 and potential occurrence of any coronary artery abnormalities in KS.

Fibroblast growth factor 23 (FGF23) gene polymorphism in children with Kawasaki syndrome (KS) and susceptibility to cardiac abnormalities