Evidence map›Paper›PMID 26427508›Full record

ArticleRheumatology international2016

Serum urate gene associations with incident gout, measured in the Framingham Heart Study, are modified by renal disease and not by body mass index.

Richard J Reynolds, Ana I Vazquez, Vinodh Srinivasasainagendra, Yann C Klimentidis, S Louis Bridges, David B Allison, Jasvinder A Singh

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Rheumatology international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. An update on the genetics of hyperuricaemia and gout.Nature reviews. Rheumatology · 2018
    Review
  4. 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

7 authors at 3 institutions in 1 country.

Richard J ReynoldsDivision of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Faculty Office Tower 805B, 510 20th Street S, Birmingham, AL, 35294, USA.
Ana I VazquezDepartment of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI, USA.
Vinodh SrinivasasainagendraDepartment of Epidemiology and Biostatistics, Michigan State University, East Lansing, MI, USA.
Yann C KlimentidisDivision of Epidemiology and Biostatistics, Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, AZ, USA.
S Louis BridgesDivision of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Faculty Office Tower 805B, 510 20th Street S, Birmingham, AL, 35294, USA.
David B AllisonNutrition Obesity Research Center, University of Alabama at Birmingham, Birmingham, AL, USA.
Jasvinder A SinghDivision of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Faculty Office Tower 805B, 510 20th Street S, Birmingham, AL, 35294, USA. Jasvinder.md@gmail.com.
University of Alabama at Birmingham · USMichigan State University · USUniversity of Arizona · US

Funding

Why is the prevalence of obesity so high in U.S. Southern States? Regional predictors of BMI and obesity treatment response.P30DK056336 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI James O Hill · 2000 to 2026
$31.9M
Multicenter Osteoarthritis Study (MOST) Second Renewal - UAB Clinical CenterU01AG018947 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LEWIS, CORA E · 2001 to 2020
$13.2M
The Effects of Urate Lowering Therapy on Inflammation, Endothelial function, andP50AR060772 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SAAG, KENNETH G · 2012 to 2021
$12.8M
Training Interventions and Genetics of Exercise Response (TIGER)R01DK062148 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BRAY, MOLLY · 2003 to 2014
$6.0M
ACOSOG Community Clinical Oncology Program (CCOP) Research BaseU10CA149950 · NCI · MAYO CLINIC ROCHESTER · PI NELSON, HEIDI, SLOAN, JEFF A. · 2011 to 2014
$3.9M
Effectiveness of DiscontinuinG bisphosphonatEs Study (EDGE)U34AR062891 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SAAG, KENNETH G · 2013 to 2014
$647k
Discovering Novel Genetic and Environmental Risk Factors for RA in African AmericK01AR060848 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI REYNOLDS, RICHARD JAMES · 2011 to 2015
$641k
Whole-Genome Prediction of Type-2 Diabetes Susceptibility in Various PopulationsK01DK095032 · NIDDK · UNIVERSITY OF ARIZONA · PI KLIMENTIDIS, YANN CHARLES · 2012 to 2014
$440k
THE FRAMINGHAM HEART STUDY-N01HC25195-268025195-268025195N01HC025195 · HC · TRUSTEES OF BOSTON UNIVERSITY · PI WOLF, PHILIP A · 2002 to 2006
–
AHRQ HHS U19 HS021110Intramural VA VA999999NCI NIH HHS U10 CA149950NHLBI NIH HHS N01 HC025195NHLBI NIH HHS N02 HL064278NIAMS NIH HHS K01 AR060848NIAMS NIH HHS P50 AR060772NIAMS NIH HHS U34 AR062891NIA NIH HHS U01 AG018947NIDDK NIH HHS K01 DK095032NIDDK NIH HHS P30 DK056336NIDDK NIH HHS R01 DK062148
6 · The paper itself

Abstract

We hypothesized that serum urate-associated SNPs, individually or collectively, interact with BMI and renal disease to contribute to risk of incident gout. We measured the incidence of gout and associated comorbidities using the original and offspring cohorts of the Framingham Heart Study. We used direct and imputed genotypes for eight validated serum urate loci. We fit binomial regression models of gout incidence as a function of the covariates, age, type 2 diabetes, sex, and all main and interaction effects of the eight serum urate SNPs with BMI and renal disease. Models were also fit with a genetic risk score for serum urate levels which corresponds to the sum of risk alleles at the eight SNPs. Model covariates, age (P = 5.95E-06), sex (P = 2.46E-39), diabetes (P = 2.34E-07), BMI (P = 1.14E-11) and the SNPs, rs1967017 (P = 9.54E-03), rs13129697 (P = 4.34E-07), rs2199936 (P = 7.28E-03) and rs675209 (P = 4.84E-02) were all associated with incident gout. No BMI by SNP or BMI by serum urate genetic risk score interactions were statistically significant, but renal disease by rs1106766 was statistically significant (P = 6.12E-03). We demonstrated that minor alleles of rs1106766 (intergenic, INHBC) were negatively associated with the risk of incident gout in subjects without renal disease, but not for individuals with renal disease. These analyses demonstrate that a significant component of the risk of gout may involve complex interplay between genes and environment.

Indexed as

Body Mass IndexGene-Environment InteractionPolymorphism, Single NucleotideAgedAged, 80 and overAge FactorsBiomarkersComorbidityFemaleGene FrequencyGenetic LociGenetic Predisposition to DiseaseGoutHumansHyperuricemiaIncidenceBiomarkersUric AcidGenetic urate scoreGout comorbiditiesMetabolic syndromeObesity

Identifiers

PMID26427508
PMCPMC4724568
OpenAlexW1871982001

What OpenQuestion holds

Textmetadata
LicenceTDM
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.