Evidence map›Paper›PMID 35907365›Full record

ArticleCytokine2022

Acute kidney injury associated to COVID-19 leads to a strong unbalance of circulant immune mediators.

Thalia Medeiros, Gabriel Macedo Costa Guimarães, Fabiana Rabe Carvalho, Lilian Santos Alves, Renan Faustino, Ana Carolina Campi-Azevedo, Vanessa Peruhype-Magalhães, Andréa Teixeira-Carvalho, Matheus de Souza Gomes, Laurence Rodrigues do Amaral and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cytokine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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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

14 authors at 3 institutions in 1 country.

Thalia MedeirosMultiuser Laboratory for Research Support in Nephrology and Medical Sciences (LAMAP), Hospital Universitario Antonio Pedro, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil; Department of Pathology, Faculty of Medicine, Universidade Federal Fluminense, Niterói, Rio de Janeiro, Brazil. Electronic address: thaliamedeiros@id.uff.br.
Gabriel Macedo Costa GuimarãesMultiuser Laboratory for Research Support in Nephrology and Medical Sciences (LAMAP), Hospital Universitario Antonio Pedro, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil.
Fabiana Rabe CarvalhoMultiuser Laboratory for Research Support in Nephrology and Medical Sciences (LAMAP), Hospital Universitario Antonio Pedro, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil.
Lilian Santos AlvesMultiuser Laboratory for Research Support in Nephrology and Medical Sciences (LAMAP), Hospital Universitario Antonio Pedro, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil.
Renan FaustinoMultiuser Laboratory for Research Support in Nephrology and Medical Sciences (LAMAP), Hospital Universitario Antonio Pedro, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil.
Ana Carolina Campi-AzevedoInstituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brazil.
Vanessa Peruhype-MagalhãesInstituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brazil.
Andréa Teixeira-CarvalhoInstituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brazil.
Matheus de Souza GomesLaboratory of Bioinformatics and Molecular Analysis (LBAM), Federal University of Uberlandia, Patos de Minas, Minas Gerais, Brazil.
Laurence Rodrigues do AmaralLaboratory of Bioinformatics and Molecular Analysis (LBAM), Federal University of Uberlandia, Patos de Minas, Minas Gerais, Brazil.
Olindo Assis Martins-FilhoInstituto René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brazil.
Jocemir Ronaldo LugonMultiuser Laboratory for Research Support in Nephrology and Medical Sciences (LAMAP), Hospital Universitario Antonio Pedro, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil; Department of Clinical Medicine - Nephrology, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil.
Jorge Reis AlmeidaMultiuser Laboratory for Research Support in Nephrology and Medical Sciences (LAMAP), Hospital Universitario Antonio Pedro, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil; Department of Clinical Medicine - Nephrology, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil.
Andrea Alice SilvaMultiuser Laboratory for Research Support in Nephrology and Medical Sciences (LAMAP), Hospital Universitario Antonio Pedro, Faculty of Medicine, Universidade Federal Fluminense, Niteroi, Rio de Janeiro, Brazil; Department of Pathology, Faculty of Medicine, Universidade Federal Fluminense, Niterói, Rio de Janeiro, Brazil. Electronic address: aasilva@id.uff.br.
Universidade Federal Fluminense · BRFundação Oswaldo Cruz · BRUniversidade Federal de Uberlândia · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSevere cases of coronavirus disease 2019 (COVID-19) have increased risk for acute kidney injury (AKI). The exacerbation of the immune response seems to contribute to AKI development, but the immunopathological process is not completely understood.

objectivesTo analyze levels of circulant immune mediators in COVID-19 patients evolving with or without AKI. We have also investigated possible associations of these mediators with viral load and clinical outcomes.

methodsThis is a longitudinal study performed with hospitalized patients with moderate to severe COVID-19. Serum levels of 27 immune mediators were measured by a multiplex immunoassay. Data were analyzed at two timepoints during the follow-up: within the first 13 days of the disease onset (early sample) and from the 14th day to death or hospital discharge (follow-up sample).

resultsWe studied 82 COVID-19 patients (59.5 ± 17.5 years, 54.9% male). Of these, 34 (41.5%) developed AKI. These patients presented higher SARS-CoV-2 viral load (P = 0.03), higher frequency of diabetes (P = 0.01) and death (P = 0.0004). Overall, AKI patients presented significantly higher and sustained levels (P < 0.05) of CCL-2, CCL-3, CCL-4, CXCL-8, CXCL-10, IFN-γ, IL-2, IL-6, TNF-α, IL-1Ra, IL-10 and VEGF. Importantly, higher levels of CCL-2, CXCL-10, IL-2, TNF-α, IL-10, FGFb, and VEGF were observed in AKI patients independently of death. ROC curves demonstrated that early alterations in CCL-2, CXCL-8, CXCL-10, IFN-γ, IL-6, IL-1Ra and IL-10 show a good predictive value regarding AKI development. Lastly, immune mediators were significantly associated with each other and with SARS-CoV-2 viral load in AKI patients.

conclusionsCOVID-19 associated AKI is accompanied by substantial alterations in circulant levels of immune mediators, which could significantly contribute to the establishment of kidney injury.

Indexed as

Acute Kidney InjuryCOVID-19FemaleHumansImmunologic FactorsInterleukin-10Interleukin 1 Receptor Antagonist ProteinInterleukin-2Interleukin-6Longitudinal StudiesMaleRetrospective StudiesRisk FactorsSARS-CoV-2Tumor Necrosis Factor-alphaVascular Endothelial Growth Factor AImmunologic FactorsInterleukin-10Interleukin 1 Receptor Antagonist ProteinInterleukin-2Interleukin-6Tumor Necrosis Factor-alphaVascular Endothelial Growth Factor AAcute kidney injuryCOVID-19CytokinesImmune mediators

Identifiers

PMID35907365
PMCPMC9309102
OpenAlexW4287094059

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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.