Evidence map›Paper›PMID 22945592›Full record

ReviewNature reviews. Rheumatology2012

The genetics of hyperuricaemia and gout.

Anthony M Reginato, David B Mount, Irene Yang, Hyon K Choi

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Rheumatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 5 pooled it
7.4field-weighted citation impact, top 2% 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

110 citing papers in PubMed, 5 syntheses or guidelines pooled it, 246 citations in OpenAlex.

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  15. Food science & nutrition · 2026
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50 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

4 authors at 3 institutions in 1 country.

Anthony M ReginatoRheumatology Division, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, 593 Eddy Street Street, Providence, RI 02903, USA.
David B Mount
Irene Yang
Hyon K Choi
Boston University · USHarvard University · USRhode Island Hospital · US

Funding

WORK DISABILITY-- PERSONS WITH RHEUMATOID ARTHRITISP60AR047785 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FELSON, DAVID TOBIN · 2001 to 2016
$18.0M
COBRE for Skeletal Health and RepairP20GM104937 · NIGMS · RHODE ISLAND HOSPITAL · PI CHEN, QIAN · 2012 to 2016
$10.8M
Genetics of GoutR01AR056291 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI CHOI, HYON K · 2008 to 2011
$2.9M
NIAMS NIH HHS P60 AR047785NIAMS NIH HHS P60AR047785NIAMS NIH HHS R01 AR056291NIAMS NIH HHS R01AR056291NIGMS NIH HHS P20 GM104937
6 · The paper itself

Abstract

Gout is a common and very painful inflammatory arthritis caused by hyperuricaemia. This review provides an update on the genetics of hyperuricaemia and gout, including findings from genome-wide association studies. Most of the genes that associated with serum uric acid levels or gout are involved in the renal urate-transport system. For example, the urate transporter genes SLC2A9, ABCG2 and SLC22A12 modulate serum uric acid levels and gout risk. The net balance between renal urate absorption and secretion is a major determinant of serum uric acid concentration and loss-of-function mutations in SLC2A9 and SLC22A12 cause hereditary hypouricaemia due to reduced urate absorption and unopposed urate secretion. However, the variance in serum uric acid explained by genetic variants is small and their clinical utility for gout risk prediction seems limited because serum uric acid levels effectively predict gout risk. Urate-associated genes and genetically determined serum uric acid levels were largely unassociated with cardiovascular-metabolic outcomes, challenging the hypothesis of a causal role of serum uric acid in the development of cardiovascular disease. Strong pharmacogenetic associations between HLA-B*5801 alleles and severe allopurinol-hypersensitivity reactions were shown in Asian and European populations. Genetic testing for HLA-B*5801 alleles could be used to predict these potentially fatal adverse effects.

Indexed as

AllopurinolATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Glucose Transport Proteins, FacilitativeGoutGout SuppressantsHumansHyperuricemiaNeoplasm ProteinsOrganic Anion TransportersOrganic Cation Transport ProteinsUric AcidABCG2 protein, humanAllopurinolATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Glucose Transport Proteins, FacilitativeGout SuppressantsNeoplasm ProteinsOrganic Anion TransportersOrganic Cation Transport ProteinsSLC22A12 protein, humanSLC2A9 protein, humanUric Acid

Identifiers

PMID22945592
PMCPMC3645862
OpenAlexW1976773608

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.