Abstract: SA-PO534
Galectin-3 and Mortality in Relation to Vascular Calcification in Incident Hemodialysis Patients
Session Information
- Hypertension and CVD: Clinical - II
November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1602 Hypertension and CVD: Clinical
Authors
- Kim, Ji Hwan, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
- Kim, Jwa-kyung, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
- Kim, Sung Gyun, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
- Jang, Jinha, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
- Kim, In Soo, Hallym University Sacred Heart Hospital, Anyang, Gyeonggi-do, Korea (the Republic of)
- Moon, Sung Jin, Catholic Kwandong University International Saint Mary's Hospital, Incheon, Korea (the Republic of)
Background
Vascular calcification is a recognized risk factor for mortality in hemodialysis patients. Galectin-3 (Gal-3), a key regulator of fibrosis, inflammation, and cell proliferation, has been implicated in adverse outcomes in several pathological conditions such as heart failure and chronic kidney disease. The study aims to determine whether elevated Gal-3 levels may affect vascular calcification and how these effects may contribute to mortality risk in hemodialysis patients.
Methods
Serum Gal-3 was measured in patients from the incident hemodialysis cohort (n=477, age 68.5 ± 12.6 years) and the cut-off value for predicting mortality was estimated by area under the receiver operating characteristic (ROC) curve (AUC). The extent of aortic arch calcification (AAC) was assessed by chest X-ray. We performed a causal mediation analysis to investigate the effect of Gal-3 on mortality via vascular calcification. Mortality data were obtained with a median follow-up of 42 months.
Results
Serum Gal-3 levels were closely associated with age (r=0.131, p=0.004), coronary artery disease history (r=0.117, p=0.010), brain natriuretic peptide levels (r=0.154, p=0.004), high-density lipoprotein (HDL) cholesterol (r=-0.176, p=0.001), high-sensitivity C-reactive protein (hs-CRP) (r=0.183, p=0.002), and AAC score (r=0.249, p<0.001). At a cut-off level of 37.0 ng/mL, the AUC for predicting mortality was 0.718 with sensitivity and specificity of 60.2% and 74.7%, respectively. Multivariate Cox regression analysis showed that higher Gal-3 levels increased all-cause mortality by 2.2-fold (95% confidence interval [CI] 1.38-3.45, p=0.001). The results of the mediation analysis suggested that this association was partially mediated by vascular calcification. Both the indirect effect between Gal-3 and mortality through vascular calcification (β=0.0068, bootstrapped 95% CI 0.0020-0.0138) and the direct effect of the Gal-3 on mortality (β=0.0370, bootstrapped 95% CI 0.0205-0.0594) were significant.
Conclusion
This study suggests a possible mechanism linking serum Gal-3 and increased mortality in hemodialysis patients, providing evidence for a significant role of Gal-3 in vascular calcification.