FGF23-niveaus correleren met vaatcalcificatie en CV-risico bij peritonealdialysepatiënten

BACKGROUND: Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone increasingly recognized as a potential contributor to cardiovascular complications in chronic kidney disease (CKD). This study investigated the association between circulating intact FGF23 levels and the severity of vascular calcification and cardiovascular event risk in peritoneal dialysis (PD) patients. MATERIALS AND METHODS: In this retrospective cohort study, we enrolled 150 PD patients treated at our center between January 2020 and January 2025. All biomarker measurements and vascular imaging data were extracted from clinically indicated chronic kidney disease-mineral and bone disorder (CKD-MBD) and cardiovascular risk assessments documented in the medical record; no additional blood sampling or CT radiation exposure was performed solely for research. FGF23 testing was clinician-initiated rather than routine, so analyses incorporated prespecified approaches to evaluate potential selection bias. Vascular calcification was assessed using complementary modalities: simple vascular calcification score (SVCS) on plain radiographs, coronary artery calcification (CAC) by computed tomography, and abdominal aortic calcification (AAC) by computed tomography. Cardiovascular events were recorded during a median follow-up of 36 months. Associations between log-transformed FGF23 and outcomes were evaluated using multivariable regression with events-per-variable monitoring, and incremental predictive value was assessed with bootstrap-validated discrimination and reclassification metrics. RESULTS: FGF23 levels were significantly and positively correlated with all three vascular calcification scores. Patients in higher FGF23 tertiles demonstrated greater vascular calcification burden and a higher cumulative incidence of cardiovascular events. In fully adjusted Cox models, each unit increase in log-transformed FGF23 was associated with a higher hazard of cardiovascular events (HR 1.74, 95% CI: 1.18 - 2.56, p = 0.005). Addition of FGF23 to a base model improved bootstrap-corrected discrimination (optimism-corrected area under the curve increment 0.024) and reclassification (category-free net reclassification improvement 0.16, p = 0.002). Attenuation of the FGF23-event association after adjustment for vascular calcification scores was consistent with partial mediation through the calcification pathway, although formal causal mediation was not performed. CONCLUSION: Elevated FGF23 levels are independently associated with greater vascular calcification burden and higher cardiovascular event risk in PD patients. FGF23 may contribute to refined cardiovascular risk stratification in this population, though prospective validation and formal mediation analyses are needed to clarify the underlying pathways.