Evidence map›Paper›PMID 35324718›Full record

ReviewToxins2022

What If Not All Metabolites from the Uremic Toxin Generating Pathways Are Toxic? A Hypothesis.

Raymond Vanholder, Sanjay K Nigam, Stéphane Burtey, Griet Glorieux

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 46 citations in OpenAlex.

  1. Novel probiotic preparation withMicrobiology spectrum · 2024
    Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. A guide to uraemic toxicity.Nature reviews. Nephrology · 2026
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 3 institutions in 3 countries.

Raymond VanholderNephrology Section, Department of Internal Medicine and Pediatrics, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0003-2633-1636
Sanjay K NigamDepartments of Pediatrics and Medicine (Nephrology), University of California San Diego, La Jolla, CA 92093, USA.
Stéphane BurteyCentre de Recherche en Cardiovasculaire et Nutrition (C2VN), Institut de la Santé et de la Recherche Médicale (INSERM), Institut National de la Recherche pour l'Agriculture, l'Alimentation et l'Environnement (INRAE), Aix Marseille University, 13005 Marseille, France.ORCID 0000-0003-1813-7884
Griet GlorieuxNephrology Section, Department of Internal Medicine and Pediatrics, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0002-7641-4707
Ghent University Hospital · BEInserm · FRUniversity of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The topic of uremic toxicity has received broad attention from the nephrological community over the past few decades. An aspect that is much less often considered is the possibility that the metabolic pathways that generate uremic toxins also may produce molecules that benefit body functions. Here, we discuss this dualism based on the example of tryptophan-derived metabolites, which comprise elements that are mainly toxic, such as indoxyl sulfate, kynurenine and kynurenic acid, but also beneficial compounds, such as indole, melatonin and indole-3-propionic acid, and ambivalent (beneficial for some aspects and harmful for others) compounds such as serotonin. This dualism can also be perceived at the level of the main receptor of the tryptophan-derived metabolites, the aryl hydrocarbon receptor (AHR), which has also been linked to both harm and benefit. We hypothesize that these beneficial effects are the reason why uremic toxin generation remained preserved throughout evolution. This duality is also not unique for the tryptophan-derived metabolites, and in this broader context we discuss the remote sensing and signaling theory (RSST). The RSST proposes that transporters (e.g., organic anion transporter 1-OAT1; ATP-binding cassette transporter G-ABCG2) and drug metabolizing enzymes form a large network of proteins interacting to promote small molecule remote communication at the inter-organ (e.g., gut-liver-heart-brain-kidney) and inter-organismal (e.g., gut microbe-host) levels. These small molecules include gut microbe-derived uremic toxins as well as beneficial molecules such as those discussed here. We emphasize that this positive side of uremic metabolite production needs more attention, and that this dualism especially needs to be considered when assessing and conceiving of therapeutic interventions. These homeostatic considerations are central to the RSST and suggest that interventions be aimed at preserving or restoring the balance between positive and negative components rather than eliminating them all without distinction.

Indexed as

Renal Insufficiency, ChronicToxins, BiologicalUremiaFemaleHumansIndicanLiverMaleTryptophanUremic ToxinsIndicanToxins, BiologicalTryptophanUremic Toxinsaryl hydrocarbon receptorgut microbiomeindoleskidney diseasekynureninesmetabolismremote sensing and signaling theorytryptophanuremiauremic toxins

Identifiers

PMID35324718
PMCPMC8953523
OpenAlexW4220864145

What OpenQuestion 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 OpenQuestion graph.