Cardiac remodeling in CKD: Diagnostic utility of circulating fibroblast growth factor‑23

Left ventricular hypertrophy (LVH) is a hallmark of uremic cardiomyopathy and a strong predictor of adverse outcomes in chronic kidney disease (CKD). Conventional biomarkers often fail to capture the full spectrum of risk, highlighting the need for novel predictors. Fibroblast growth factor‑23 (FGF‑23) has been implicated in pathological cardiac remodeling through FGFR4‑dependent signaling pathways. This study aimed to evaluate the diagnostic utility of circulating FGF‑23 for cardiac remodeling, particularly Left ventricular hypertrophy, in non‑dialysis CKD patients. A cross‑sectional observational study was conducted between October 2024 and April 2025 in Thi‑Qar, Iraq. Participants included 89 patients with CKD stage 3 to 5, 40 patients with heart failure, and 37 healthy controls. Demographic, clinical, biochemical, and echocardiographic data were collected. Serum FGF‑23 was measured using enzyme-linked immunosorbent assay. Associations with cardiac remodeling were assessed using logistic regression models with sequential adjustments. Diagnostic performance was evaluated by receiver operating characteristic curve analysis. Serum FGF‑23 was significantly higher in CKD and heart failure groups compared to controls. Among CKD patients, FGF‑23 levels were elevated in those with cardiac remodeling (164.9 vs 133.4 pg/mL). Receiver operating characteristic analysis yielded an area under the curve of 0.723, with an optimal cutoff of >164.8 pg/mL (sensitivity, 50.9%; specificity, 96.7%). Multivariate regression confirmed FGF-23 as an independent risk factor for remodeling across all adjustment models (odds ratio range, 1.021-1.039; P < .01). Circulating FGF-23 is independently associated with cardiac remodeling in non-dialysis CKD patients. Its high specificity suggests potential utility as a biomarker for cardiovascular risk stratification, complementing traditional measures.