Evidence map›Paper›PMID 39140866›Full record

ArticleClinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis

Endogenous Dysregulation of Thromboinflammatory Biomarkers in End-Stage Renal Disease, and Their Amplification by Heart Failure.

Vanessa Robbin, Vinod Bansal, Fakiha Siddiqui, Madeline Allen, Debra Hoppensteadt-Moorman, Bulent Kantarcioglu, Emma Abulencia, Evangeline Magpoc, Jawed Fareed, Mushabbar Syed

Abstract read
In one paragraph

Article in Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. miR-29a-3p/Renal failure · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Vanessa RobbinDepartment of Vascular Biology and Hemostasis, Cardiovascular Research Institute, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.ORCID 0009-0009-6270-9895
Vinod BansalDepartment of Nephrology, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.
Fakiha SiddiquiDepartment of Vascular Biology and Hemostasis, Cardiovascular Research Institute, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.
Madeline AllenDepartment of Vascular Biology and Hemostasis, Cardiovascular Research Institute, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.
Debra Hoppensteadt-MoormanDepartment of Vascular Biology and Hemostasis, Cardiovascular Research Institute, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.ORCID 0000-0001-9342-4213
Bulent KantarciogluDepartment of Vascular Biology and Hemostasis, Cardiovascular Research Institute, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.ORCID 0000-0003-3060-721X
Emma AbulenciaDepartment of Nephrology, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.
Evangeline MagpocDepartment of Nephrology, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.
Jawed FareedDepartment of Vascular Biology and Hemostasis, Cardiovascular Research Institute, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.ORCID 0000-0003-3465-2499
Mushabbar SyedDepartment of Cardiology, Health Sciences Division, Loyola University Chicago, Maywood, IL, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In patients with end-stage renal disease (ESRD), heart failure with reduced ejection fraction (HFrEF) is a common comorbidity. Thromboinflammatory processes in both conditions represent complex pathophysiology, demonstrated by dysregulation of thromboinflammatory biomarkers, and commonly resulting in the combined pathology of cardiorenal syndrome. We sought to investigate the effects of HFrEF on these biomarkers in patients with ESRD, and observe the relationship to mortality. Blood samples from 73 patients with ESRD (mean age 67 ± 13 years, 56% male) and 40 healthy controls were analyzed via enzyme-linked immunosorbent assay and other chromogenic methods for angiopoietin-2 (Ang2), endogenous glycosaminoglycans, fatty acid binding protein, interleukin-6, lipopolysaccharide, free fatty acids, NT-pro B-type natriuretic peptide, tumor necrosis factor α, vascular endothelial growth factor, and von Willebrand factor. Patients were stratified into those with or without HFrEF (EF < 50%). Patients had highly prevalent comorbidities including coronary artery disease 46%, diabetes 69%, hypertension 97%, and smoking 49%. Most biomarkers were upregulated in ESRD compared to controls. Patients with HFrEF and ESRD had greater interleukin-6 and NT-pro B-type natriuretic peptide and lesser lipopolysaccharide compared to ESRD only. Spearman correlations between most biomarkers were increased in HFrEF + ESRD over ESRD only. Ang-2 was associated with mortality in this cohort. The dysregulation of thromboinflammation in ESRD is somewhat amplified in comorbid HFrEF. Correlation among biomarkers in this cohort indicates the mechanisms of thromboinflammatory biomarker generation in ESRD and HFrEF share an integrative process. Ang2, interleukin-6, and lipopolysaccharide show promise as biomarkers for risk stratification among patients with both HFrEF and ESRD.

Indexed as

BiomarkersHeart FailureKidney Failure, ChronicAgedFemaleHumansInflammationMaleMiddle AgedBiomarkersbiomarkerscardiovascular diseaseendothelial dysfunctionend-stage renal diseaseheart failureinflammation

Identifiers

PMID39140866
PMCPMC11325466

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.