Evidence map›Paper›PMID 26572664›Full record

ReviewJournal of nephrology2016

Role of IgA receptors in the pathogenesis of IgA nephropathy.

Sebastian M Lechner, Christina Papista, Jonathan M Chemouny, Laureline Berthelot, Renato C Monteiro

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  8. Article
  9. Article
  10. Review
  11. Review
  12. The Role of IgA in the Pathogenesis of IgA Nephropathy.International journal of molecular sciences · 2019
    Review
  13. Secondary IgA nephropathy.Kidney international · 2018
    Review
  14. Review
  15. New insights into the pathogenesis of IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2018
    Review
  16. Article
  17. Biomarkers and targeted new therapies for IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2017
    Review
  18. Review
  19. Review
  20. 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

5 authors at 4 institutions in 1 country.

Sebastian M LechnerInstitut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149 Centre de Recherche sur l'Inflammation, Paris, France.
Christina PapistaInstitut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149 Centre de Recherche sur l'Inflammation, Paris, France.
Jonathan M ChemounyInstitut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149 Centre de Recherche sur l'Inflammation, Paris, France.
Laureline BerthelotInstitut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149 Centre de Recherche sur l'Inflammation, Paris, France.
Renato C MonteiroInstitut National de la Santé et de la Recherche Médicale (INSERM) UMR 1149 Centre de Recherche sur l'Inflammation, Paris, France. renato.monteiro@inserm.fr.
Sorbonne Paris Cité · FRCentre de Recherche sur l'Inflammation · FRInserm · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin A nephropathy (IgAN) or Berger's disease is the most common form of primary glomerulonephritis in the world and one of the first causes of end-stage renal failure. IgAN is characterized by the accumulation of immune complexes containing polymeric IgA1 in mesangial areas. The pathogenesis of this disease involves the deposition of polymeric and hypogalactosylated IgA1 (Gd-IgA1) in the mesangium. Quantitative and structural changes of Gd-IgA1 play a key role in the development of the disease due to functional abnormalities of two IgA receptors: the FcαRI (CD89) expressed by blood myeloid cells and the transferrin receptor (CD71) on mesangial cells. Abnormal Gd-IgA1 induces release of soluble CD89, which participates in the formation of circulating IgA1 complexes. These complexes are trapped by CD71 that is overexpressed on mesangial cells in IgAN patients together with the crosslinking enzyme transglutaminase 2 allowing pathogenic IgA complex formation in situ and mesangial cell activation. A humanized mouse model expressing IgA1 and CD89 develops IgAN in a similar manner as patients. In this model, a food antigen, the gliadin, was shown to be crucial for circulating IgA1 complex formation and deposition, which could be prevented by a gluten-free diet. Identification of these new partners opens new therapeutic prospects for IgAN treatment.

Indexed as

AnimalsAntigens, CDCeliac DiseaseDiet, Gluten-FreeDisease Models, AnimalGliadinGlomerulonephritis, IGAHumansImmunoglobulin AKidney GlomerulusLigandsReceptors, FcReceptors, TransferrinSignal TransductionAntigens, CDCD71 antigenFc(alpha) receptorGliadinIgA receptorImmunoglobulin ALigandsReceptors, FcReceptors, TransferrinCD89GlutenIgA glycosylationIgA nephropathyIgA receptorsPrimary glomerulonephritis

Identifiers

PMID26572664
OpenAlexW2227709405

What OpenQuestion holds

Textmetadata
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.