Evidence map›Paper›PMID 29324897›Full record

ArticlePloS one2018

Serum galactose-deficient-IgA1 and IgG autoantibodies correlate in patients with IgA nephropathy.

William J Placzek, Hiroyuki Yanagawa, Yuko Makita, Matthew B Renfrow, Bruce A Julian, Dana V Rizk, Yusuke Suzuki, Jan Novak, Hitoshi Suzuki

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
4.9field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

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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

9 authors at 2 institutions in 2 countries.

William J PlaczekDepartment of Biochemistry and Molecular Genetics, The University of Alabama at Birmingham, Birmingham, Alabama, United States of America.ORCID 0000-0003-4096-8617
Hiroyuki YanagawaDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Yuko MakitaDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Matthew B RenfrowDepartment of Biochemistry and Molecular Genetics, The University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Bruce A JulianDepartment of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Dana V RizkDepartment of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Yusuke SuzukiDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Jan NovakDepartment of Microbiology, The University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Hitoshi SuzukiDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
University of Alabama at Birmingham · USJuntendo University · JP

Funding

Elucidating IgA Nephropathy through Genetic Studies of IgA1 GlycosylationR01DK082753 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GHARAVI, ALI G, NOVAK, JAN · 2009 to 2024
$8.7M
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR01DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JAN NOVAK · 2007 to 2026
$6.0M
Analytical tools for the analysis of clustered O-glycans in clinical samplesR01GM098539 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RENFROW, MATTHEW B · 2011 to 2019
$2.7M
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR56DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NOVAK, JAN · 2012 to 2012
$92k
NIDDK NIH HHS R01 DK078244NIDDK NIH HHS R01 DK082753NIDDK NIH HHS R56 DK078244NIGMS NIH HHS R01 GM098539NIH HHS DK078244NIH HHS GM098539
6 · The paper itself

Abstract

IgA nephropathy is an autoimmune disease characterized by IgA1-containing glomerular immune deposits. We previously proposed a multi-hit pathogenesis model in which patients with IgA nephropathy have elevated levels of circulatory IgA1 with some O-glycans deficient in galactose (Gd-IgA1, autoantigen). Gd-IgA1 is recognized by anti-glycan IgG and/or IgA autoantibodies, resulting in formation of pathogenic immune complexes. Some of these immune complexes deposit in the kidney, activate mesangial cells, and incite glomerular injury leading to clinical presentation of IgA nephropathy. Several studies have demonstrated that elevated circulatory levels of either Gd-IgA1 or the corresponding autoantibodies predict progressive loss of renal clearance function. In this study we assessed a possible association between serum levels of Gd-IgA1 and IgG or IgA autoantibodies specific for Gd-IgA1 in serum samples from 135 patients with biopsy-proven IgA nephropathy, 76 patients with other renal diseases, and 106 healthy controls. Our analyses revealed a correlation between the concentrations of the autoantigen and the corresponding IgG autoantibodies in sera of patients with IgA nephropathy, but not of disease or healthy controls. Moreover, our data suggest that IgG is the predominant isotype of Gd-IgA1-specific autoantibodies in IgA nephropathy. This work highlights the importance of both initial hits in the pathogenesis of IgA nephropathy.

Indexed as

AutoantibodiesBiomarkersCohort StudiesEnzyme-Linked Immunosorbent AssayGlomerulonephritis, IGAHumansImmunoglobulin AImmunoglobulin GRenal Insufficiency, ChronicAutoantibodiesBiomarkersImmunoglobulin AImmunoglobulin G

Identifiers

PMID29324897
PMCPMC5764330
OpenAlexW2782628349

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.