Abstract: FR-PO0370
Translational Insights into Predictive Biomarker Trajectories for eGFR Decline and Major Adverse Kidney Events After Acute Myocardial Infarction
Session Information
- Hypertension and CVD: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1602 Hypertension and CVD: Clinical
Authors
- Lee, Chia Ying, National Taiwan University College of Medicine, Taipei City, Taiwan
- Tsai, Ping-Chi, National Taiwan University Hospital, Taipei City, Taiwan
- Huang, Yue-Jhu, National Taiwan University Hospital, Taipei City, Taiwan
- See, Daniel H. W., National Taiwan University College of Medicine, Taipei City, Taiwan
- Huang, Jenq-wen, National Taiwan University College of Medicine, Taipei City, Taiwan
- Su, Chi-Ting, National Taiwan University College of Medicine, Taipei City, Taiwan
Background
Acute myocardial infarction (AMI) not only endangers cardiovascular health but also accelerates kidney damage, leading to progressive renal dysfunction and major adverse kidney events (MAKE). Identifying predictive biomarkers and clinical factors is critical for mitigating these risks and advancing precision medicine.
Methods
A cohort of 25 AMI patients (<75 years) was analyzed, excluding those on dialysis or with active infections. Biomarkers (FABP3, LTBP4, NGAL-MMP9) were measured at baseline (prior to AMI-related catheterization), 1 month, and 1 year post-AMI. A murine model validated biomarker trajectories and explored the link between myocardial injury and renal fibrosis. Generalized estimating equations (GEE) assessed associations between biomarkers and cystatin C-based eGFR trajectories, while regression identified MAKE predictors.
Results
The cohort (mean age: 64.2 ± 12.2 years; 68% male) included 28% with chronic kidney disease (CKD) and 44% with diabetes. GEE analysis identified male sex (OR: −2.18, p=0.020), atrial fibrillation (OR: −14.26, p<0.001), and liver cirrhosis (OR: −12.24, p<0.001) as predictors of faster eGFR decline, while younger age (≤53 years, OR: 4.62, p<0.001) and ARB/ACEI therapy (OR: 7.97, p<0.001) were associated with improved outcomes. Biomarker thresholds predicting favorable outcomes included FABP3 <2370.60 ng/mL (OR: 1.64, p=0.011), NGAL-MMP9 <28.49 ng/mL (OR: 7.83, p<0.001), and LTBP4 levels between 1.021–2.335 ng/mL (OR: 5.99, p<0.001). Patients with pre-AMI eGFR 60–90 mL/min/1.73 m2 and HbA1c <8% showed reduced MAKE risk (HR: 7.19, p=0.0019). Plasma LTBP4 and NGAL-MMP9 were strongly associated with increased MAKE risk (p<0.001). In the murine model, severe AMI was linked to elevated FABP3 and renal fibrosis (p<0.001), reinforcing a mechanistic link between myocardial injury and renal impairment.
Conclusion
This study establishes FABP3, LTBP4, and NGAL-MMP9 as critical biomarkers for predicting renal trajectories post-AMI, bridging the gap between myocardial injury and kidney dysfunction. By uncovering these biomarker thresholds and their clinical implications, the findings pave the way for targeted interventions that align with precision medicine, offering hope for improved management of high-risk populations prone to MAKE and eGFR decline.