Evidence map›Paper›PMID 40461059›Full record

ArticleGut2025

Toxic microbiome and progression of chronic kidney disease: insights from a longitudinal CKD-Microbiome Study.

Manolo Laiola, Laetitia Koppe, Amine Larabi, Florence Thirion, Céline Lange, Benoit Quinquis, Aymeric David, Emmanuelle Le Chatelier, Berengere Benoit, Giuseppina Sequino and 14 more

Abstract read
In one paragraph

Article in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
–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

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Gut microbes · 2026
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  20. Gut-kidney axis: Dysbiosis and renal disease.World journal of nephrology · 2026
    Review
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

24 authors.

Manolo Laiola *Université Paris-Saclay, INRAE, MGP, Jouy-en-Josas, France.
Laetitia Koppe *Department of Nephrology, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, Pierre-Bénite, France.ORCID 0000-0002-5076-2420
Amine LarabiDepartment of Pharmacology and Toxicology, Raymond Poincaré Hospital, AP-HP, Garches; Centre for Research in Epidemiology and Population Health (CESP), Team MOODS, Inserm UMRS 1018, UVSQ-Paris-Saclay University, Montigny-le-Bretonneux, France.
Florence ThirionUniversité Paris-Saclay, INRAE, MGP, Jouy-en-Josas, France.ORCID 0000-0002-2310-5548
Céline LangeCentre for Research in Epidemiology and Population Health (CESP), Paris-Saclay University, Versailles Saint Quentin University, INSERM UMRS 1018, Clinical Epidemiology Team, Villejuif, France.
Benoit QuinquisUniversité Paris-Saclay, INRAE, MGP, Jouy-en-Josas, France.
Aymeric DavidUniversité Paris-Saclay, INRAE, MGP, Jouy-en-Josas, France.
Emmanuelle Le ChatelierUniversité Paris-Saclay, INRAE, MGP, Jouy-en-Josas, France.
Berengere BenoitUniv. Lyon, CarMeN lab, INSERM U1060, INRA, Université Claude Bernard Lyon 1, Pierre-Bénite, France.
Giuseppina SequinoDepartment of Agricultural Sciences, University of Naples Federico II, Portici, Italy.
Stephanie ChanonUniv. Lyon, CarMeN lab, INSERM U1060, INRA, Université Claude Bernard Lyon 1, Pierre-Bénite, France.
Aurelie Vieille-MarchisetUniv. Lyon, CarMeN lab, INSERM U1060, INRA, Université Claude Bernard Lyon 1, Pierre-Bénite, France.
Yves-Edouard HerpeBiobanque de Picardie, Amiens University Hospital, Amiens, France.
Jean-Claude AlvarezDepartment of Pharmacology and Toxicology, Raymond Poincaré Hospital, AP-HP, Garches; Centre for Research in Epidemiology and Population Health (CESP), Team MOODS, Inserm UMRS 1018, UVSQ-Paris-Saclay University, Montigny-le-Bretonneux, France.
Griet GlorieuxDepartment of Internal Medicine, Nephrology Unit, Ghent University Hospital, Ghent, Belgium.
Hubert KrukowskiDepartment of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, Leuven, Belgium.
Geert Rb HuysDepartment of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, Leuven, Belgium.
Jeroen RaesDepartment of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, Leuven, Belgium.
Denis FouqueDepartment of Nephrology, Hospices Civils de Lyon, Centre Hospitalier Lyon-Sud, Pierre-Bénite, France.
Ziad A MassyCentre for Research in Epidemiology and Population Health (CESP), Paris-Saclay University, Versailles Saint Quentin University, INSERM UMRS 1018, Clinical Epidemiology Team, Villejuif, France.
Stanislav Dusko Ehrlich *Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK.ORCID 0000-0002-7563-4046
Bénédicte Stengel *Centre for Research in Epidemiology and Population Health (CESP), Paris-Saclay University, Versailles Saint Quentin University, INSERM UMRS 1018, Clinical Epidemiology Team, Villejuif, France.
Sandra Wagner *Universite de Lorraine, INSERM CIC 1433, Nancy CHRU, Inserm U1116 DCAC, FCRIN INI-CRCT, Nancy, France s.wagner2@chru-nancy.fr.ORCID 0000-0002-3251-3754
CKD-REIN Study collaborators

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe gut microbiota has been linked to non-communicable diseases, including chronic kidney disease (CKD). However, the relationships between gut microbiome composition changes, uraemic toxins (UTs) accumulation, and diet on CKD severity and progression remain underexplored.

objectiveTo characterise relationships between gut microbiome composition and functionality, UTs diet, and CKD severity and progression, as well as assess microbial contributions to UTs accumulation through mice faecal microbiota transplantation (FMT).

designThis study profiled the gut microbiome of 240 non-dialysis patients with CKD (CKD-REIN cohort) using shotgun metagenomics, with follow-up in 103 patients after 3 years, with comparisons with healthy volunteers from the

resultsCompared with matched healthy controls, patients with CKD exhibited gut microbiota alteration, with enrichment of UT precursor-producing species. Patients with severe CKD exhibited higher UT levels and greater enrichment of UT (precursor)-producing species in the microbiota than patients with moderate CKD. Over time, UT (precursor)-producing species increased, and a plant-based low protein diet appeared to mitigate these changes. FMT from patients with CKD to antibiotic-treated CKD model mice increased serum UT levels and exacerbated kidney fibrosis.

conclusionsThis study highlights the role of the microbiome and UTs in CKD, suggesting a potential therapeutic target to slow disease progression.

Indexed as

Gastrointestinal MicrobiomeRenal Insufficiency, ChronicUremic ToxinsAdultAgedAnimalsDietDisease ProgressionFecal Microbiota TransplantationFemaleHumansLongitudinal StudiesMaleMetagenomicsMiceMiddle AgedUremic ToxinsEPIDEMIOLOGYMICROBIOME

Identifiers

PMID40461059
PMCPMC12505076

What OpenQuestion holds

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LicenceCC BY-NC
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 OpenQuestion graph.