Evidence map›Paper›PMID 40711156›Full record

ReviewToxins2025

Increased Cardiovascular Mortality in Hemodialysis: The Role of Chronic Inflammation, Complement Activation, and Non-Biocompatibility.

Ákos Géza Pethő, Tibor Fülöp, Petronella Orosz, Gábor Szénási, Mihály Tapolyai, László Dézsi

Abstract readReview
In one paragraph

Review in Toxins, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
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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

6 authors.

Ákos Géza PethőDepartment of Internal Medicine and Oncology, Faculty of Medicine, Semmelweis University, 1000 Budapest, Hungary.ORCID 0000-0001-9776-9841
Tibor FülöpMedicine Service, Ralph H. Johnson VA Medical Center, Charleston, SC 29401, USA.ORCID 0000-0002-3346-7040
Petronella OroszBethesda Children's Hospital, 1146 Budapest, Hungary.
Gábor SzénásiInstitute of Translational Medicine, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0002-7350-6091
Mihály TapolyaiMedicine Service, Ralph H. Johnson VA Medical Center, Charleston, SC 29401, USA.ORCID 0000-0002-2915-3962
László DézsiInstitute of Translational Medicine, Semmelweis University, 1085 Budapest, Hungary.ORCID 0000-0002-4190-9793

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic kidney disease (CKD) is an established global health problem, with the increased prevalence of vascular inflammation, accelerated atherogenesis, and thrombotic risk all contributing to overall cardiovascular risk. The major CKD-specific risk factor is presumed to be the accumulation of uremic toxins in circulation and tissues, further accelerating the progression of CKD and its co-morbidities, including those of bone mineral disorders and cardiovascular diseases. MATERIALS AND

methodsIn our narrative review, we focused on non-traditional cardiovascular risk factors, as they evolve with declined kidney function and are potentially further modulated by the choice of kidney replacement therapy.

resultsBased on the data from the literature to date, the pre-eminent role of non-traditional risk factors emerges to mediate inflammation and increased cardiovascular mortality. In particular, patients receiving hemodialysis (HD) display dramatically increased CVD-mediated mortality. This intensified state of inflammation may be linked to the direct exposure of the bloodstream to a bio-incompatible environment in HD; for both complement-mediated and non-complement-mediated reactions, the possible contribution of neutrophil extracellular traps and complement activation-related pseudoallergy are reviewed in detail.

conclusionsOur narrative review emphasizes key elements of a bio-incompatible HD environment that may contribute to increased cardiovascular mortality in patients receiving HD. Summarizing these results may provide conceptual opportunities to develop new therapeutic targets.

Indexed as

Cardiovascular DiseasesComplement ActivationInflammationRenal DialysisRenal Insufficiency, ChronicAnimalsHumansbiocompatibilitychronic inflammationcomplement activationhemodialysisimmunologicalmortalityperitoneal dialysis

Identifiers

PMID40711156
PMCPMC12297944

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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.