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Abstract: SA-PO391

Thromboinflammatory Biomarkers and Their Relationship With Circulating Glycosaminoglycans in ESRD Patients

Session Information

Category: Dialysis

  • 701 Dialysis: Hemodialysis and Frequent Dialysis

Authors

  • Bansal, Vinod K., Loyola University Health System, Maywood, Illinois, United States
  • Allen, Madeline T., Loyola University Health System, Maywood, Illinois, United States
  • Siddiqui, Fakiha, Loyola University Health System, Maywood, Illinois, United States
  • Hoppensteadt, Debra, Loyola University Health System, Maywood, Illinois, United States
  • Krupa, Emily G., Loyola University Health System, Maywood, Illinois, United States
  • Kantarcioglu, Bulent, Loyola University Health System, Maywood, Illinois, United States
  • Fareed, Jawed, Loyola University Health System, Maywood, Illinois, United States
Background

End stage renal disease (ESRD) is a complex progressive medical condition that affects multiple organ systems. Given the high risk of morbidity and mortality of ESRD as well as its rising incidence, it is critical to understand the relevance of thromboinflammatory biomarkers in disease development and progression of kidney dysfunction. The purpose of this study is to profile the levels of thromboinflammatory biomarkers in ESRD patients including D-Dimer, C-reactive protein (CRP), von Willebrand factor (vWF), plasminogen activator inhibitor 1 (PAI-1), and thrombin activatable fibrinolysis inhibitor (TAFI). In addition, the levels of anti-PF4 IgG and endogenous circulating glycosaminoglycans (GAGs) were measured.

Methods

Citrated plasma samples were collected from seventy-three ESRD patients. Control plasma samples (NHP) from healthy, non-smoking adults aged 19 to 53 were obtained commercially. Validated ELISA methods have been used to profile each of the biomarkers. The levels of endogenous GAGs were determined (Redprobes UG, Germany). To compare the levels of thromboinflammatory biomarkers, anti-PF4 IgG, and endogenous GAGs in different groups, appropriate statistical methods included Mann-Whitney U, t-tests, Kruskal-Wallis ANOVA and experiment correlation analysis methods were performed.

Results

All of the biomarkers and GAGs were significantly elevated in the ESRD patients, with the exception of TAFI (p < 0.05). The ESRD patients exhibited varying levels of increase in the D-Dimer, CRP, vWF, PAI-1, anti-PF4 IgG, and GAG levels (p < 0.05). D-Dimer showed the most pronounced increase (1075%) followed by PAI-1 (361.31%), anti-PF4 IgG (209.78%), CRP (101.77%) and endogenous GAGs (17.29%). The correlation analysis revealed varying degrees of association among these biomarker levels, in particular the endogenous GAGs and PAI-1.

Conclusion

These results suggest that thromboinflammatory biomarkers offer the potential utility of identifying inflammation in end-stage renal disease. Marked increase in thromboinflammatory mediators due to endothelial damage may result in the upregulation of glycosaminoglycans and may contribute to platelet activation and vascular dysregulation.

Funding

  • Clinical Revenue Support