1. The Association of Fgf23 and Inflammation in Heart Failure with Normal Kidney Function
- Author
-
Bernhard Koller, Ulmer H, Dörler J, Dünser M, Grander W, Polzl G, and Zaruba MM
- Subjects
medicine.medical_specialty ,education.field_of_study ,Cardiac output ,Ejection fraction ,biology ,business.industry ,Population ,C-reactive protein ,Cardiomyopathy ,Renal function ,urologic and male genital diseases ,medicine.disease ,stomatognathic diseases ,Internal medicine ,Heart failure ,biology.protein ,Cardiology ,Medicine ,business ,education ,Survival analysis - Abstract
Background: Fibroblast growth factor-23 produced by osteocytes regulates calcium and phosphate homeostasis which are cornerstones for bone integrity. Recently, FGF23 was also found to be directly related with both severity and prognosis of heart failure. However, the mechanism of FGF23 regulation in heart failure, particularly in patients with preserved renal function is poorly understood. Methods: In this retrospective single center trial we assessed the association of systemic inflammation (surrogated by CRP) and FGF23 regulation in 221 stable non-ischemic heart failure patients (age ≥ 18) with reduced ejection fraction and an estimated glomerular filtration rate of more than 60 ml/min/1.73m². Furthermore, we analyzed the prognostic ability of FGF23 and CRP in this population. Fasting ct-FGF23, highly sensitive CRP and a comprehensive panel of further biomarkers, as well as invasive hemodynamic measures from right heart catheterization, were used for univariate and multivariate regression analysis. Results: In bivariate correlation analysis ct-FGF23 was correlated with Cardiac output (r= -0.42); NTproBNP (r=0.34) and CRP (r=0.31); for all of those p < 0.001. Multivariate linear regression analysis revealed CRP and CO as independently associated with ct-FGF23 (total model fit; r²=0.32; p
- Published
- 2019
- Full Text
- View/download PDF