Evidence map›Paper›PMID 37425258›Full record

ArticleFrontiers in pediatrics2023

Assessment of interleukin-10 promoter variant (-1082A/G) and cytokine production in patients with hemolytic uremic syndrome.

Micaela Aldana Mongelos, Fernando Nicolás Sosa, Gonzalo Ezequiel Pineda, Gabriela Fiorentino, Adriana Santiago, Miguel Martín Abelleyro, Liliana Carmen Rossetti, Ramón Exeni, Carlos Daniel De Brasi, Marina Sandra Palermo and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pediatrics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Associations ofBiomedicines · 2026
    Article
  2. 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

11 authors at 2 institutions in 1 country.

Micaela Aldana MongelosLaboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental (CONICET)-Academia Nacional de Medicina, Buenos Aires, Argentina.
Fernando Nicolás SosaLaboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental (CONICET)-Academia Nacional de Medicina, Buenos Aires, Argentina.
Gonzalo Ezequiel PinedaLaboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental (CONICET)-Academia Nacional de Medicina, Buenos Aires, Argentina.
Gabriela FiorentinoLaboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental (CONICET)-Academia Nacional de Medicina, Buenos Aires, Argentina.
Adriana SantiagoDepartamento de Nefrología, Diálisis y Trasplante, Hospital del Niño Prof. Dr. Ramón Exeni, San Justo, Argentina.
Miguel Martín AbelleyroLaboratorio de Genética Molecular de la Hemofilia, Instituto de Medicina Experimental (CONICET)-Academia Nacional de Medicina, Buenos Aires, Argentina.
Liliana Carmen RossettiLaboratorio de Genética Molecular de la Hemofilia, Instituto de Medicina Experimental (CONICET)-Academia Nacional de Medicina, Buenos Aires, Argentina.
Ramón ExeniDepartamento de Nefrología, Diálisis y Trasplante, Hospital del Niño Prof. Dr. Ramón Exeni, San Justo, Argentina.
Carlos Daniel De BrasiLaboratorio de Genética Molecular de la Hemofilia, Instituto de Medicina Experimental (CONICET)-Academia Nacional de Medicina, Buenos Aires, Argentina.
Marina Sandra PalermoLaboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental (CONICET)-Academia Nacional de Medicina, Buenos Aires, Argentina.
María Victoria RamosLaboratorio de Patogénesis e Inmunología de Procesos Infecciosos, Instituto de Medicina Experimental (CONICET)-Academia Nacional de Medicina, Buenos Aires, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARAcademia Nacional de Medicina · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Hemolytic uremic syndrome (HUS) is a condition that results in acute kidney failure mainly in children, which is caused by Shiga toxin-producing Methods: Plasma and peripheral blood mononuclear cells (PBMC) were collected from healthy children and HUS patients exhibiting hemolytic anemia, thrombocytopenia, and kidney damage. Monocytes identified as CD14 Results: Circulating IL-10 levels were increased in HUS patients, but PBMC from these patients exhibited a lower capacity to secrete this cytokine compared with those from healthy children. Interestingly, there was a negative association between the circulating levels of IL-10 and inflammatory cytokine IL-8. We observed that circulating IL-10 levels were threefold higher in HUS patients with -1082G allele in comparison to AA genotype. Moreover, there was relative enrichment of GG/AG genotypes in HUS patients with severe kidney failure. Discussion: Our results suggest a possible contribution of SNP -1082 (A/G) to the severity of kidney failure in HUS patients that should be further evaluated in a larger cohort.

Indexed as

HUSIL-10monocytesrenal failureSNP

Identifiers

PMID37425258
PMCPMC10327435
OpenAlexW4381853225

What Socratic holds

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LicenceCC BY
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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.