PB0034 - Endogenous dysregulation of biomarkers of thromboinflammatory responses in end-stage renal disease, and their amplification by heart failure

Sunday, June 25, 2023

18:30 – 19:30 ET

Room: Exhibition

Co-Author(s)

VR

Vanessa Robbin, BS

Medical student
Loyola University Medical Center
Maywood, Illinois, United States

Co-Author(s)

VB

Vinod Bansal

Doctor
Loyola University Medical Center
Maywood, Illinois, United States

Presenting Author(s)

Fakiha Siddiqui, PhD Candidate

PhD Candidate
Department of Pathology and Laboratory Medicine, Cardiovascular Research Institute, Loyola University Chicago, Health Sciences Division, Maywood, IL, USA.
Maywood, Illinois, United States

Co-Author(s)

Madeline Allen, BS

Research Associate
Loyola University Medical Center
Naperville, Illinois, United States
JF

Jawed Fareed, n/a

Professor
Loyola University Medical Center
MAYWOOD, Illinois, United States
MS

Mushabbar Syed

Doctor
Loyola University Medical Center
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.

Aims: This study sought 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.

Conclusion(s): The dysregulation of thromboinflammatory biomarkers in ESRD-HD is somewhat amplified in comorbid HFrEF. Better correlation among biomarkers in this cohort indicates the mechanisms of thromboinflammatory biomarker generation have an integrative process that is shared between the two conditions.