Evidence map›Paper›PMID 25945405›Full record

ArticleKidney international2015

IgM exacerbates glomerular disease progression in complement-induced glomerulopathy.

Sarah E Panzer, Jennifer Laskowski, Brandon Renner, Liudmila Kulik, Danica Ljubanovic, Kendra M Huber, Weixiong Zhong, Matthew C Pickering, V Michael Holers, Joshua M Thurman

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 54 citations in OpenAlex.

  1. B-cell-targeting therapies in podocytopathies.Pediatric nephrology (Berlin, Germany) · 2026
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 3 countries.

Sarah E PanzerDivision of Nephrology, Department of Medicine, University of Wisconsin Madison, Madison, Wisconsin, USA.
Jennifer LaskowskiDepartment of Medicine, University of Colorado Denver, Aurora, Colorado, USA.
Brandon RennerDepartment of Medicine, University of Colorado Denver, Aurora, Colorado, USA.
Liudmila KulikDepartment of Medicine, University of Colorado Denver, Aurora, Colorado, USA.
Danica LjubanovicDepartment of Pathology, University Hospital Dubrava, Zagreb, Croatia.
Kendra M HuberDepartment of Medicine, University of Colorado Denver, Aurora, Colorado, USA.
Weixiong ZhongDepartment of Pathology, University of Wisconsin Madison, Madison, Wisconsin, USA.
Matthew C PickeringCentre for Complement and Inflammation Research, Imperial College, London, UK.
V Michael HolersDepartment of Medicine, University of Colorado Denver, Aurora, Colorado, USA.
Joshua M ThurmanDepartment of Medicine, University of Colorado Denver, Aurora, Colorado, USA.
University of Colorado Denver · USUniversity of Wisconsin–Madison · USCentre for Inflammation Research · GBUniversity Hospital Dubrava · HR

Funding

The Complement System and Ischemic Acute Renal FailureR01DK076690 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Joshua M Thurman · 2008 to 2026
$6.6M
Role of IgM and Complement Activation in Glomerular DiseaseF32DK096711 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI PANZER, SARAH E · 2012 to 2012
$60k
NIDDK NIH HHS F32 DK096711NIDDK NIH HHS F32DK096711-01NIDDK NIH HHS R01 DK076690Wellcome Trust 098476
6 · The paper itself

Abstract

Although glomerular immunoglobulin M (IgM) deposition occurs in a variety of glomerular diseases, the mechanism of deposition and its clinical significance remain controversial. Some have theorized IgM becomes passively trapped in areas of glomerulosclerosis. However, recent studies found that IgM specifically binds damaged glomeruli. Therefore, we tested whether natural IgM binds to neo-epitopes exposed after insults to the glomerulus and exacerbates disease in mice deficient in the complement regulatory protein factor H; a model of non-sclerotic and nonimmune-complex glomerular disease. Immunofluorescence microscopy demonstrated mesangial and capillary loop deposition of IgM, whereas ultrastructural analysis found IgM deposition on endothelial cells and subendothelial areas. Factor H-deficient mice lacking B cells were protected from renal damage, as evidenced by milder histologic lesions on light and electron microscopy. IgM, but not IgG, from wild-type mice bound to cultured murine mesangial cells. Furthermore, injection of purified IgM into mice lacking B cells bound within the glomeruli and induced proteinuria. A monoclonal natural IgM-recognizing phospholipids also bound to glomeruli in vivo and induced albuminuria. Thus, our results indicate specific IgM antibodies bind to glomerular epitopes and that IgM contributes to the progression of glomerular damage in this mouse model of non-sclerotic glomerular disease.

Indexed as

Complement ActivationAlbuminuriaAnimalsAntibody SpecificityB-LymphocytesCell LineComplement Factor HDisease Models, AnimalDisease ProgressionEpitopesGlomerulonephritisImmunoglobulin MKidney GlomerulusMaleMice, Inbred C57BLMice, KnockoutComplement Factor HEpitopesImmunoglobulin M

Identifiers

PMID25945405
PMCPMC4556608
OpenAlexW1663880144

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.