Evidence map›Paper›PMID 42043039›Full record

ArticleToxins2026

Kidney Function Modulates Gut Microbial Metabolism.

Mara Lauriola, Sophie Valkenburg, Sander Dejongh, Ward Zadora, Hubert Krukowski, Pieter Evenepoel, Jeroen Raes, Ricard Farré, Griet Glorieux, Björn Meijers

Abstract read
In one paragraph

Article in Toxins, 2026. 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
–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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Mara LauriolaNephrology and Renal Transplantation Research Group, Department of Microbiology, Immunology and Transplantation, KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0001-9563-7757
Sophie ValkenburgNephrology Section, Department of Internal Medicine and Paediatrics, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0003-3019-550X
Sander DejonghNephrology and Renal Transplantation Research Group, Department of Microbiology, Immunology and Transplantation, KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0002-5359-3028
Ward ZadoraNephrology and Renal Transplantation Research Group, Department of Microbiology, Immunology and Transplantation, KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0002-9958-3474
Hubert KrukowskiLaboratory of Molecular Bacteriology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, KU Leuven, 3000 Leuven, Belgium.
Pieter EvenepoelNephrology and Renal Transplantation Research Group, Department of Microbiology, Immunology and Transplantation, KU Leuven, 3000 Leuven, Belgium.
Jeroen RaesLaboratory of Molecular Bacteriology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, KU Leuven, 3000 Leuven, Belgium.
Ricard FarréTranslational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0001-7158-171X
Griet GlorieuxNephrology Section, Department of Internal Medicine and Paediatrics, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0002-7641-4707
Björn MeijersNephrology and Renal Transplantation Research Group, Department of Microbiology, Immunology and Transplantation, KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0002-2846-2026

Funding

European Union's Horizon 2020 research and innovation program 860329
6 · The paper itself

Abstract

Growing evidence suggests that chronic kidney disease (CKD) profoundly disrupts gut microbiome and its activity. This study explores how CKD affects colon microbial metabolism, focusing on (1) the representativeness of fecal metabolomics, (2) saccharolytic and proteolytic fermentation metabolites, and (3) the gut microbiome's role in the partitioning of tryptophan in its metabolic pathways. Tryptophan's main metabolic pathways include the indolic and the kynurenine pathways, which lead, respectively, to the formation of indoxyl sulfate and kynurenine, both contributing to uremic toxicity. Using a rat model of CKD, we evaluated whether fecal concentrations of microbial compounds, on which most studies are based, reflect the colonic concentrations in contact with the gut mucosa. Thus, we quantified the concentration and content of amino acids, indole, p-cresol, and also short-chain fatty acids, in different colon sections. We demonstrated that CKD promotes increased proteolytic fermentation and an augmented tryptophan partitioning into both the indolic and kynurenine pathways. Depletion of the indolic pathway obtained upon antibiotic treatment leads to a further enhancement of the kynurenine pathway.

Indexed as

ColonGastrointestinal MicrobiomeKidneyRenal Insufficiency, ChronicAnimalsFatty Acids, VolatileFecesFermentationIndolesKynurenineMaleRats, WistarTryptophanFatty Acids, VolatileIndolesKynurenineTryptophanchronic kidney diseasecolon proteolytic fermentationgut–kidney axisgut microbiotatargeted metabolite analysestryptophan

Identifiers

PMID42043039
PMCPMC13119667

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.