Evidence map›Paper›PMID 27513517›Full record

ArticlePloS one2016

Association of FMO3 Variants and Trimethylamine N-Oxide Concentration, Disease Progression, and Mortality in CKD Patients.

Cassianne Robinson-Cohen, Richard Newitt, Danny D Shen, Allan E Rettie, Bryan R Kestenbaum, Jonathan Himmelfarb, Catherine K Yeung

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 7 pooled it
5.4field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 7 syntheses or guidelines pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Trial
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    Review
  18. Review
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  20. Coding Variants of theReports of biochemistry & molecular biology · 2022
    Article
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

7 authors at 1 institution in 1 country.

Cassianne Robinson-CohenKidney Research Institute, Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington, 98195, United States of America.
Richard NewittKidney Research Institute, Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington, 98195, United States of America.
Danny D ShenDepartment of Pharmacy, School of Pharmacy, University of Washington, Seattle, Washington, 98195, United States of America.
Allan E RettieDepartment of Medicinal Chemistry, School of Pharmacy, University of Washington, Seattle, Washington, 98195, United States of America.
Bryan R KestenbaumKidney Research Institute, Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington, 98195, United States of America.
Jonathan HimmelfarbKidney Research Institute, Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington, 98195, United States of America.
Catherine K YeungKidney Research Institute, Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington, 98195, United States of America.
University of Washington · US

Funding

NCCIH Supplement to NCATS/CTSA Program for KL2 Scholars - M. SoddersKL2TR002317 · NCATS · UNIVERSITY OF WASHINGTON · PI Christy Michelle McKinney · 2017 to 2026
$14.5M
Institute of Translational Health SciencesKL2TR000421 · NCATS · UNIVERSITY OF WASHINGTON · PI DISIS, MARY L. · 2012 to 2016
$12.6M
NCATS NIH HHS KL2 TR000421NCATS NIH HHS KL2 TR002317
6 · The paper itself

Abstract

Elevated levels of circulating pro-atherogenic uremic solutes, particularly trimethylamine N-oxide (TMAO), have been implicated in cardiovascular disease development in patients with chronic kidney disease (CKD). TMAO is generated from trimethylamine (TMA) via metabolism by hepatic flavin-containing monooxygenase isoform 3 (FMO3). We determined the functional effects of three common FMO3 variants at amino acids 158, 308, and 257 on TMAO concentrations in a prospective cohort study and evaluated associations of polymorphisms with CKD progression and mortality. Each additional minor allele at amino acid 158 was associated with a 0.38 μg/mL higher circulating TMAO (p = 0.01) and with faster rates of annualized relative eGFR decline. Participants with 0, 1 and 2 variant alleles averaged an eGFR loss of 8%, 12%, and 14% per year, respectively (p-for trend = 0.05). Compared to participants with the homozygous reference allele, heterozygous and homozygous variant participants had a 2.0-fold (95% CI: 0.85, 4.6) and 2.2-fold (95% CI: 0.89, 5.48) higher risk of mortality, respectively (p-for-trend = 0.04). No associations with clinical outcomes were observed for allelic variants at amino acids 257 or 308. Understanding the contribution of genetic variation of FMO3 to disease progression and all-cause mortality can guide recommendations for diet modification or pharmacotherapy in CKD patients at increased risk of adverse outcomes.

Indexed as

BiomarkersDisease ProgressionFemaleHumansMaleMethylaminesMiddle AgedOxygenasesPolymorphism, Single NucleotidePrognosisProspective StudiesRenal Insufficiency, ChronicSurvival RateBiomarkersdimethylaniline monooxygenase (N-oxide forming)MethylaminesOxygenasestrimethyloxamine

Identifiers

PMID27513517
PMCPMC4981377
OpenAlexW2507227271

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.