Evidence map›Paper›PMID 30029499›Full record

ReviewToxins2018

Impact of Altered Intestinal Microbiota on Chronic Kidney Disease Progression.

Esmeralda Castillo-Rodriguez, Raul Fernandez-Prado, Raquel Esteras, Maria Vanessa Perez-Gomez, Carolina Gracia-Iguacel, Beatriz Fernandez-Fernandez, Mehmet Kanbay, Alberto Tejedor, Alberto Lazaro, Marta Ruiz-Ortega and 4 more

Registry-linked trialAbstract readReview
In one paragraph

Review in Toxins, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04689074 (Costituzione Della Biobanca Del Microbiota Intestinale e Salivare Umano), which is not on this map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing 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.

NCT04689074 completednot on this mapstarted 2021, after this paper: background citation

Costituzione Della Biobanca Del Microbiota Intestinale e Salivare Umano: Dalla Disbiosi Alla Simbiosi

TypeobservationalSponsorAzienda Ospedaliero-Universitaria Consorziale Policlinico di BariRan2021 to 2022Enrolled150ConditionsAutosomal Dominant Polycystic Kidney Disease (ADPKD), Advanced-Chronic Kidney Disease (CKD), Diabetic Kidney Disease (DKD), IgA Nephropathy (IgAN)ArmsBiological sample collection, Questionnaire, Medical examination
3 · Its place in the literature

Who cites it

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

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Disulfiram Attenuates Adenine-Induced Renal Fibrosis by Modulating Inflammatory and Immunometabolic Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Article
  7. Review
  8. Gut-kidney axis: Dysbiosis and renal disease.World journal of nephrology · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

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

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.

Esmeralda Castillo-RodriguezNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. ecastillor@quironsalud.es.
Raul Fernandez-PradoNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. raul.fernandezp@quironsalud.es.
Raquel EsterasNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. raquel.esteras@quironsalud.es.
Maria Vanessa Perez-GomezNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. mvanessa@fjd.es.
Carolina Gracia-IguacelNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. CGraciaI@quironsalud.es.
Beatriz Fernandez-FernandezNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. bfernandez@fjd.es.
Mehmet KanbayDepartment of Internal Medicine, Koc University School of Medicine, Istanbul 34450, Turkey. drkanbay@yahoo.com.
Alberto TejedorNefrología, IIS-Gregorio Marañón, Universidad Complutense de Madrid, 28007 Madrid, Spain. atejedor@senefro.org.
Alberto LazaroNefrología, IIS-Gregorio Marañón, Universidad Complutense de Madrid, 28007 Madrid, Spain. alazaro10@gmail.com.
Marta Ruiz-OrtegaNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. mruizo@quironsalud.es.
Emilio Gonzalez-ParraNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. egparra@quironsalud.es.
Ana B SanzNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. asanz@fjd.es.
Alberto OrtizNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. aortiz@fjd.es.ORCID 0000-0002-9805-9523
Maria Dolores Sanchez-NiñoNephrology Department, IIS-Fundación Jiménez Díaz-Universidad Autónoma de Madrid, 28040 Madrid, Spain. mdsanchez@fjd.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In chronic kidney disease (CKD), accumulation of uremic toxins is associated with an increased risk of CKD progression. Some uremic toxins result from nutrient processing by gut microbiota, yielding precursors of uremic toxins or uremic toxins themselves, such as trimethylamine N-Oxide (TMAO), p-cresyl sulphate, indoxyl sulphate and indole-3 acetic acid. Increased intake of some nutrients may modify the gut microbiota, increasing the number of bacteria that process them to yield uremic toxins. Circulating levels of nutrient-derived uremic toxins are associated to increased risk of CKD progression. This offers the opportunity for therapeutic intervention by either modifying the diet, modifying the microbiota, decreasing uremic toxin production by microbiota, increasing toxin excretion or targeting specific uremic toxins. We now review the link between nutrients, microbiota and uremic toxin with CKD progression. Specific focus will be placed on the generation specific uremic toxins with nephrotoxic potential, the decreased availability of bacteria-derived metabolites with nephroprotective potential, such as vitamin K and butyrate and the cellular and molecular mechanisms linking these toxins and protective factors to kidney diseases. This information provides a conceptual framework that allows the development of novel therapeutic approaches.

Indexed as

Gastrointestinal MicrobiomeAnimalsDisease ProgressionHumansInflammationIntestinal MucosaPermeabilityRenal Insufficiency, ChronicToxins, BiologicalToxins, Biologicalcarnitinecholinechronic kidney diseasegut-kidney axisindoxyl sulphatemicrobiotap-cresyl sulphatetrimethylamine N-Oxidetryptophantyrosine

Identifiers

PMID30029499
PMCPMC6070989

What OpenQuestion holds

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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.