Evidence map›Paper›PMID 32408613›Full record

ReviewInternational journal of molecular sciences2020

Molecular Mechanisms of Premature Aging in Hemodialysis: The Complex Interplay Between Innate and Adaptive Immune Dysfunction.

Vincenzo Losappio, Rossana Franzin, Barbara Infante, Giulia Godeas, Loreto Gesualdo, Alberto Fersini, Giuseppe Castellano, Giovanni Stallone

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% of its field
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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

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  20. Association between B-cell activating factor and future depressive symptoms in hemodialysis patients.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) · 2025
    Observational
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

8 authors at 2 institutions in 1 country.

Vincenzo LosappioNephrology, Dialysis and Transplantation Unit, Department of Medical and Surgical Sciences, University of Foggia, 71100 Foggia, Italy.
Rossana FranzinNephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.
Barbara InfanteNephrology, Dialysis and Transplantation Unit, Department of Medical and Surgical Sciences, University of Foggia, 71100 Foggia, Italy.
Giulia GodeasNephrology, Dialysis and Transplantation Unit, Department of Medical and Surgical Sciences, University of Foggia, 71100 Foggia, Italy.
Loreto GesualdoNephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy.
Alberto FersiniGeneral Surgery Units, Department of Medical and Surgical Sciences, University of Foggia, 71100 Foggia, Italy.
Giuseppe CastellanoNephrology, Dialysis and Transplantation Unit, Department of Medical and Surgical Sciences, University of Foggia, 71100 Foggia, Italy.
Giovanni StalloneNephrology, Dialysis and Transplantation Unit, Department of Medical and Surgical Sciences, University of Foggia, 71100 Foggia, Italy.
University of Foggia · ITUniversity of Bari Aldo Moro · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hemodialysis (HD) patient are known to be susceptible to a wide range of early and long-term complication such as chronic inflammation, infections, malnutrition, and cardiovascular disease that significantly affect the incidence of mortality. A large gap between the number of people with end-stage kidney disease (ESKD) and patients who received kidney transplantation has been identified. Therefore, there is a huge need to explore the underlying pathophysiology of HD complications in order to provide treatment guidelines. The immunological dysregulation, involving both the innate and adaptive response, plays a crucial role during the HD sessions and in chronic, maintenance treatments. Innate immune system mediators include the dysfunction of neutrophils, monocytes, and natural killer (NK) cells with signaling mediated by NOD-like receptor P3 (NLRP3) and Toll-like receptor 4 (TLR4); in addition, there is a significant activation of the complement system that is mediated by dialysis membrane-surfaces. These effectors induce a persistent, systemic, pro-inflammatory, and pro-coagulant milieu that has been described as inflammaging. The adaptive response, the imbalance in the CD4+/CD8+ T cell ratio, and the reduction of Th2 and regulatory T cells, together with an altered interaction with B lymphocyte by CD40/CD40L, have been mainly implicated in immune system dysfunction. Altogether, these observations suggest that intervention targeting the immune system in HD patients could improve morbidity and mortality. The purpose of this review is to expand our understanding on the role of immune dysfunction in both innate and adaptive response in patients undergoing hemodialysis treatment.

Indexed as

Adaptive ImmunityAging, PrematureAnimalsCardiovascular DiseasesHumansImmune System DiseasesImmunity, InnateInflammationKidney Failure, ChronicRenal Dialysiscomplementhemodialysiskidneypremature aging

Identifiers

PMID32408613
PMCPMC7279398
OpenAlexW3025509810

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.