Evidence map›Paper›PMID 25542908›Full record

Observational studyClinical journal of the American Society of Nephrology : CJASN2015

Mapping novel immunogenic epitopes in IgA nephropathy.

Sang Hoon Woo, Tara K Sigdel, Van T Dinh, Minh-Thien Vu, Minnie M Sarwal, Richard A Lafayette

Open access · bronzeAbstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in Clinical journal of the American Society of Nephrology : CJASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact, top 85% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Autoimmunity in IgA nephropathy.Frontiers in immunology · 2026
    Review
  3. Article
  4. Article
  5. Noninvasive Urinary Monitoring of Progression in IgA Nephropathy.International journal of molecular sciences · 2019
    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

6 authors at 3 institutions in 1 country.

Sang Hoon WooDivision of Hospital Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania;
Tara K SigdelDepartment of Surgery, University of California, San Francisco, California;
Van T DinhDepartment of Surgery, University of California, San Francisco, California;
Minh-Thien VuDepartment of Surgery, University of California, San Francisco, California;
Minnie M SarwalDepartment of Surgery, University of California, San Francisco, California; czar@stanford.edu minnie.sarwal@ucsfmedctr.org.
Richard A LafayetteDivision of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford University, Stanford, California czar@stanford.edu minnie.sarwal@ucsfmedctr.org.
University of California, San Francisco · USStanford University · USThomas Jefferson University Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesIgA plays a key role in IgA nephropathy (IgAN) by forming immune complexes and depositing in the glomeruli, leading to an inflammatory response. However, the antigenic targets and functional characterization of IgA have been incompletely defined in this disease. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This study was performed in sera from patients who were studied as part of a prospective, observational study of IgAN. These patients (n=22) all had biopsy-proven IgAN within 3 years of study initiation, complete clinical data, annual urinary inulin clearance for GFRs, and at least 5 years of follow-up. Progression was defined as loss of >5 ml/min per 1.73 m(2) per year of inulin clearance measured over at least 5 years. A protein microarray was used for detection of IgAN-specific IgA autoantibodies in blood across approximately 9000 human antigens to specifically identify the most immunogenic protein targets that drive IgA antibodies in IgAN (n=22), healthy controls (n=10), and non-IgAN glomerular diseases (n=17). Results were validated by ELISA assays in sera and by immunohistochemistry in IgAN kidney biopsies. IgA-specific antibodies were correlated with clinical and histologic variables to assess their effect on disease progression and prognosis.

resultsFifty-four proteins mounted highly significant IgA antibody responses in patients with IgAN with a false discovery rate (q value) of ≤10%; 325 antibodies (P≤0.05) were increased overall. Antitissue transglutaminase IgA was significantly elevated in IgAN (P<0.001, q value of 0%). IgA antibodies to DDX4 (r=-0.55, P=0.01) and ZADH2 (r=-0.48, P=0.02) were significantly correlated with the decline of renal function. Specific IgA autoantibodies are elevated in IgAN compared with normal participants and those with other glomerular diseases.

conclusionsIn this preliminary study, IgA autoantibodies target novel proteins, highly expressed in the kidney glomerulus and tubules. These IgA autoantibodies may play important roles in the pathogenesis of IgAN.

Indexed as

Epitope MappingEpitopesAdultAntigens, SurfaceArea Under CurveAutoantibodiesBlood ProteinsCase-Control StudiesDEAD-box RNA HelicasesDisease ProgressionDNA-Binding ProteinsFemaleGlomerular Filtration RateGlomerulonephritis, IGAGTP-Binding ProteinsHomeodomain ProteinsAntigens, SurfaceARIH2 protein, humanAutoantibodiesBlood ProteinsDDX4 protein, humanDEAD-box RNA HelicasesDNA-Binding ProteinsEpitopesGTP-Binding ProteinsHomeodomain ProteinsImmunoglobulin AMembrane ProteinsMPP1 protein, humanMuscle ProteinsNerve Tissue ProteinsPOLR2M protein, humanProtein Glutamine gamma Glutamyltransferase 2RNA Polymerase IISIX2 protein, humanTEAD4 protein, humanTEA Domain Transcription FactorsTranscription FactorsTransglutaminasesUbiquitin-Protein LigasesZADH2 protein, humanIgA nephropathynephritisprimary GN

Identifiers

PMID25542908
PMCPMC4348675
OpenAlexW2155511502

What OpenQuestion holds

Textmetadata
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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.