Abstract: FR-PO395
Dysregulation of Thrombo-Inflammatory Biomarkers in ESRD and Their Potentiation with Heart Failure
Session Information
- Hypertension and CVD: Basic
November 03, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1601 Hypertension and CVD: Basic
Authors
- Robbin, Vanessa, Loyola University Medical Center, Maywood, Illinois, United States
- Siddiqui, Fakiha, Loyola University Medical Center, Maywood, Illinois, United States
- Nikolovski, Srdjan, Loyola University Medical Center, Maywood, Illinois, United States
- Allen, Madeline T., Loyola University Medical Center, Maywood, Illinois, United States
- Fareed, Jawed, Loyola University Medical Center, Maywood, Illinois, United States
- Bansal, Vinod K., Loyola University Medical Center Department of Nephrology, Maywood, Illinois, United States
Background
In patients with end-stage renal disease undergoing hemodialysis (ESRD-HD), heart failure with reduced ejection fraction (HFrEF) represents a common comorbidity. Thromboinflammatory processes in both ESRD and HFrEF represent complex pathophysiology, and are demonstrated by dysregulation of thromboinflammatory biomarkers. This study aims to investigate the effects of HFrEF as a comorbidity on these biomarkers in ESRD-HD patients.
Methods
Blood samples from 71 ESRD-HD patients and 40 healthy normal controls were analyzed via commercial ELISA and other chromogenic methods for levels of angiopoietin-2, endogenous glycosaminoglycans, FABP, IL-6, LPS, free fatty acids, proBNP, TNFa, VEGF, Vit D, and vWF. Patient groups were stratified into those with or without HFrEF (EF<50%) in the 6 months prior or following the plasma collection using echocardiography records obtained via chart review.
Results
Compared to ESRD-HD alone, a significant increase (p < 0.05) was noted in IL-6 and proBNP, in those with ESRD-HD and HFrEF. Notably, Spearman’s rank correlations were compiled for both groups, and markedly stronger correlations were noted in those with both ESRD-HD and HFrEF. Moreover, PAI-1 and tPA were higher in HFrEF group, suggesting the fibrinolytic deficit.
Conclusion
The dysregulation of thrombo-inflammatory biomarkers in ESRD-HD is amplified in comorbid HFrEF. Correlation among biomarkers in this cohort indicates the mechanisms of thrombo-inflammatory biomarker generation have an integrative process that is shared between the two conditions. The role of fibrinolytic deficit is to be further investigated.