Evidence map›Paper›PMID 34069405›Full record

ReviewToxins2021

Dysbiosis-Related Advanced Glycation Endproducts and Trimethylamine N-Oxide in Chronic Kidney Disease.

Kensei Taguchi, Kei Fukami, Bertha C Elias, Craig R Brooks

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
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  11. Article
  12. Review
  13. Role of Trimethylamine N-Oxide in Heart Failure.Reviews in cardiovascular medicine · 2024
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. [Gut-derived uremic toxin trimethylamine-N-oxide in cardiovascular disease under end-stage renal disease: an injury mechanism and therapeutic target].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2022
    Review
  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 2 institutions in 2 countries.

Kensei TaguchiDivision of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN 37232, USA.ORCID 0000-0002-5555-1809
Kei FukamiDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, Kurume 830-0011, Japan.
Bertha C EliasDivision of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Craig R BrooksDivision of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Vanderbilt University Medical Center · USKurume University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a public health concern that affects approximately 10% of the global population. CKD is associated with poor outcomes due to high frequencies of comorbidities such as heart failure and cardiovascular disease. Uremic toxins are compounds that are usually filtered and excreted by the kidneys. With the decline of renal function, uremic toxins are accumulated in the systemic circulation and tissues, which hastens the progression of CKD and concomitant comorbidities. Gut microbial dysbiosis, defined as an imbalance of the gut microbial community, is one of the comorbidities of CKD. Meanwhile, gut dysbiosis plays a pathological role in accelerating CKD progression through the production of further uremic toxins in the gastrointestinal tracts. Therefore, the gut-kidney axis has been attracting attention in recent years as a potential therapeutic target for stopping CKD. Trimethylamine N-oxide (TMAO) generated by gut microbiota is linked to the progression of cardiovascular disease and CKD. Also, advanced glycation endproducts (AGEs) not only promote CKD but also cause gut dysbiosis with disruption of the intestinal barrier. This review summarizes the underlying mechanism for how gut microbial dysbiosis promotes kidney injury and highlights the wide-ranging interventions to counter dysbiosis for CKD patients from the view of uremic toxins such as TMAO and AGEs.

Indexed as

Gastrointestinal MicrobiomeAnimalsCardiovascular DiseasesDisease ProgressionDysbiosisGlycation End Products, AdvancedHumansMethylaminesRenal Insufficiency, ChronicGlycation End Products, AdvancedMethylaminestrimethyloxamineAGEschronic kidney diseasedysbiosisgut microbiotaRAGETMAO

Identifiers

PMID34069405
PMCPMC8158751
OpenAlexW3165086355

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.