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GDF-15, Galectin 3, Soluble ST2, and Risk of Mortality and Cardiovascular Events in CKD
Courtney Tuegel1, Ronit Katz2, Mariam Alam1
1Department of Medicine, University of Washington, Seattle, WA.
Insights
Higher levels of Growth Differentiation Factor 15 (GDF-15), galectin 3 (Gal-3), and soluble ST2 (sST2) in patients with chronic kidney disease (CKD) are linked to increased mortality. Elevated GDF-15 also predicts heart failure risk.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Biomarker Research
Background:
- Patients with chronic kidney disease (CKD) face an elevated risk of cardiovascular disease (CVD).
- Inflammation, cardiac remodeling, and fibrosis are implicated in CKD-associated CVD.
- Growth differentiation factor 15 (GDF-15), galectin 3 (Gal-3), and soluble ST2 (sST2) are potential biomarkers for these pathways in CKD.
Purpose of the Study:
- To investigate the association between circulating GDF-15, Gal-3, and sST2 levels and adverse cardiovascular outcomes in individuals with CKD.
- To determine if these biomarkers predict all-cause mortality, heart failure hospitalizations, and atherosclerotic CVD events.
Main Methods:
- An observational cohort study involving 883 participants with CKD from two multicenter cohorts.
- Baseline measurements of circulating GDF-15, Gal-3, and sST2 were taken.
- Cox proportional hazards models were used to assess the association of each biomarker with outcomes, adjusting for relevant covariates.
Main Results:
- Higher concentrations of GDF-15, Gal-3, and sST2 were significantly associated with increased all-cause mortality in CKD patients.
- Elevated GDF-15 levels were also associated with a higher risk of heart failure hospitalization.
- No significant associations were found between these biomarkers and atherosclerotic CVD events.
Conclusions:
- Circulating GDF-15, Gal-3, and sST2 are significant predictors of mortality in individuals with CKD.
- GDF-15 may serve as a specific biomarker for heart failure risk in this population.
- Further research is needed to understand the underlying mechanisms connecting these biomarkers to CVD in CKD.
Rationale & Objective:
Inflammation, cardiac remodeling, and fibrosis may explain in part the excess risk for cardiovascular disease (CVD) in patients with chronic kidney disease (CKD). Growth differentiation factor 15 (GDF-15), galectin 3 (Gal-3), and soluble ST2 (sST2) are possible biomarkers of these pathways in patients with CKD.
Study Design:
Observational cohort study.
Setting & Participants:
Individuals with CKD enrolled in either of 2 multicenter CKD cohort studies: the Seattle Kidney Study or C-PROBE (Clinical Phenotyping and Resource Biobank Study).
Exposures:
Circulating GDF-15, Gal-3, and sST2 measured at baseline.
Outcomes:
Primary outcome was all-cause mortality. Secondary outcomes included hospitalization for physician-adjudicated heart failure and the atherosclerotic CVD events of myocardial infarction and cerebrovascular accident.
Analytic Approach:
Cox proportional hazards models used to test the association of each biomarker with each outcome, adjusting for demographics, CVD risk factors, and kidney function.
Results:
Among 883 participants, mean estimated glomerular filtration rate was 49±19mL/min/1.73m2. Higher GDF-15 (adjusted HR [aHR] per 1-SD higher, 1.87; 95% CI, 1.53-2.29), Gal-3 (aHR per 1-SD higher, 1.51; 95% CI, 1.36-1.78), and sST2 (aHR per 1-SD higher, 1.36; 95% CI, 1.17-1.58) concentrations were significantly associated with mortality. Only GDF-15 level was also associated with heart failure events (HR per 1-SD higher, 1.56; 95% CI, 1.12-2.16). There were no detectable associations between GDF-15, Gal-3, or sST2 concentrations and atherosclerotic CVD events.
Limitations:
Event rates for heart failure and atherosclerotic CVD were low.
Conclusions:
Adults with CKD and higher circulating GDF-15, Gal-3, and sST2 concentrations experienced greater mortality. Elevated GDF-15 concentration was also associated with an increased rate of heart failure. Further work is needed to elucidate the mechanisms linking these circulating biomarkers with CVD in patients with CKD.
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