학술논문
Fibroblast Growth Factor 23 and Risk of Heart Failure Subtype: The CRIC (Chronic Renal Insufficiency Cohort) Study
Document Type
article
Author
Alexander S. Leidner; Xuan Cai; Leila R. Zelnick; Jungwha Lee; Nisha Bansal; Andreas Pasch; Mayank Kansal; Jing Chen; Amanda Hyre Anderson; James H. Sondheimer; James P. Lash; Raymond R. Townsend; Alan S. Go; Harold I. Feldman; Sanjiv J. Shah; Myles Wolf; Tamara Isakova; Rupal C. Mehta; Lawrence J. Appel, MD, MPH; Jing Chen, MD, MMSc, MSc; Debbie L. Cohen, MD; Harold I. Feldman, MD, MSCE; Alan S. Go, MD; James P. Lash, MD; Robert G. Nelson, MD, PhD, MS; Mahboob Rahman, MD; Panduranga S. Rao, MD; Vallabh O. Shah, PhD, MS; Mark L. Unruh, MD, MS
Source
Kidney Medicine, Vol 5, Iss 11, Pp 100723- (2023)
Subject
Language
English
ISSN
2590-0595
Abstract
Rationale & Objective: Heart failure (HF) is an important cause of morbidity and mortality among individuals with chronic kidney disease (CKD). A large body of evidence from preclinical and clinical studies implicates excess levels of fibroblast growth factor 23 (FGF23) in HF pathogenesis in CKD. It remains unclear whether the relationship between elevated FGF23 levels and HF risk among individuals with CKD varies by HF subtype. Study Design: Prospective cohort study. Settings & Participants: A total of 3,502 participants were selected in the Chronic Renal Insufficiency Cohort study. Exposure: Baseline plasma FGF23. Outcomes: Incident HF by subtype and total rate of HF hospitalization. HF was categorized as HF with preserved ejection fraction (HFpEF, ejection fraction [EF] ≥ 50%), HF with reduced EF (HFrEF, EF