Evidence map›Paper›PMID 25589612›Full record

ArticleJournal of the American Society of Nephrology : JASN2015

Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion.

Vinicius Andrade-Oliveira, Mariane T Amano, Matheus Correa-Costa, Angela Castoldi, Raphael J F Felizardo, Danilo C de Almeida, Enio J Bassi, Pedro M Moraes-Vieira, Meire I Hiyane, Andrea C D Rodas and 9 more

2 registry-linked trialsOpen access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 292 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
292citing papers in PubMed, 7 pooled it
14.9field-weighted citation impact, top 1% 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.

NCT02976688 phase2 / phase3unknown statusnot on this mapstarted 2017, after this paper: background citation

Effects of Short-chain Fatty Acids, Here Sodium Propionate, a Metabolism Product of the Human Gut-microbiome, on Inflammatory and Metabolic Parameters in Patients on Maintenance Hemodialysis - a Pilot Study

TypeinterventionalSponsorAzienda Sanitaria ASL Avellino 2Ran2017 to 2017Enrolled15ConditionsEndstage Renal DiseaseArmsSodium Propionate
NCT07443280 narecruitingnot on this mapstarted 2026, after this paper: background citation

Alterations of Gut Derived Uremic Toxins and Microbiome Metabolites by Multispecies Synbiotic Supplementation in Hemodialysis Patients

TypeinterventionalSponsorTungs' Taichung Metroharbour HospitalRan2026 to 2026Enrolled30ConditionsSymbiotic, Uremic Toxins, Gut -MicrobiotaArmsMultispecies Synbiotic Supplementation
3 · Its place in the literature

Who cites it

292 citing papers in PubMed, 7 syntheses or guidelines pooled it, 485 citations in OpenAlex.

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232 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 6 institutions in 2 countries.

Vinicius Andrade-OliveiraLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Mariane T AmanoLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Matheus Correa-CostaLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Angela CastoldiLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Raphael J F FelizardoNephrology Division, Federal University of São Paulo, São Paulo, Brazil;
Danilo C de AlmeidaNephrology Division, Federal University of São Paulo, São Paulo, Brazil;
Enio J BassiLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Pedro M Moraes-VieiraLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Meire I HiyaneLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Andrea C D RodasLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Jean P S PeronNeuroimmune Interactions Laboratory, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Cristhiane F AguiarLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil;
Marlene A ReisDivision of Pathology, Universidade Federal do Triângulo Mineiro, Uberaba, Brazil;
Willian R RibeiroDepartment of Pharmacy and Biotechnology, Universidade Anhanguera de São Paulo UNIAN-SP, São Paulo, Brazil;
Claudete J ValdugaDepartment of Pharmacy and Biotechnology, Universidade Anhanguera de São Paulo UNIAN-SP, São Paulo, Brazil;
Rui CuriDepartment of Physiology and Biophysics, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil; and.
Marco Aurelio Ramirez VinoloDepartment of Genetics, Evolution and Bioagents, Institute of Biology, University of Campinas-UNICAMP, São Paulo, Brazil.
Caroline M FerreiraDepartment of Physiology and Biophysics, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil; and.
Niels Olsen Saraiva CâmaraLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, São Paulo, Brazil; Nephrology Division, Federal University of São Paulo, São Paulo, Brazil; niels@icb.usp.br.
Universidade de São Paulo · BRInstitute of Biomedical Science · GBAnhanguera-Uniderp University · BRUniversidade Federal de São Paulo · BRUniversidade Estadual de Campinas (UNICAMP) · BRUniversidade Federal do Triângulo Mineiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Short-chain fatty acids (SCFAs) are fermentation end products produced by the intestinal microbiota and have anti-inflammatory and histone deacetylase-inhibiting properties. Recently, a dual relationship between the intestine and kidneys has been unraveled. Therefore, we evaluated the role of SCFA in an AKI model in which the inflammatory process has a detrimental role. We observed that therapy with the three main SCFAs (acetate, propionate, and butyrate) improved renal dysfunction caused by injury. This protection was associated with low levels of local and systemic inflammation, oxidative cellular stress, cell infiltration/activation, and apoptosis. However, it was also associated with an increase in autophagy. Moreover, SCFAs inhibited histone deacetylase activity and modulated the expression levels of enzymes involved in chromatin modification. In vitro analyses showed that SCFAs modulated the inflammatory process, decreasing the maturation of dendritic cells and inhibiting the capacity of these cells to induce CD4(+) and CD8(+) T cell proliferation. Furthermore, SCFAs ameliorated the effects of hypoxia in kidney epithelial cells by improving mitochondrial biogenesis. Notably, mice treated with acetate-producing bacteria also had better outcomes after AKI. Thus, we demonstrate that SCFAs improve organ function and viability after an injury through modulation of the inflammatory process, most likely via epigenetic modification.

Indexed as

Acute Kidney InjuryAnimalsBifidobacteriumCell LineDendritic CellsDrug Evaluation, PreclinicalFatty Acids, VolatileInflammationMaleMice, Inbred C57BLOxidative StressProbioticsReperfusion InjuryFatty Acids, Volatileepigenetic modificationsischemia-reperfusionkidney diseasemicrobiotaSCFA

Identifiers

PMID25589612
PMCPMC4520159
OpenAlexW2127826587

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.