Evidence map›Paper›PMID 34300307›Full record

ReviewJournal of clinical medicine2021

History of IgA Nephropathy Mouse Models.

Batoul Wehbi, Virginie Pascal, Lina Zawil, Michel Cogné, Jean-Claude Aldigier

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. IgA nephropathy: gut microbiome regulates the production of hypoglycosilated IgA1 via the TLR4 signaling pathway.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Article
  7. Review
  8. IgA nephropathy.Nature reviews. Disease primers · 2023
    Review
  9. Review
  10. Article
  11. 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

5 authors at 2 institutions in 1 country.

Batoul WehbiImmunology Department, UMR CNRS 7276 INSERM 1262, Limoges University, 87032 Limoges, France.
Virginie PascalImmunology Department, UMR CNRS 7276 INSERM 1262, Limoges University, 87032 Limoges, France.
Lina ZawilImmunology Department, UMR CNRS 7276 INSERM 1262, Limoges University, 87032 Limoges, France.
Michel CognéImmunology Department, EFS Bretagne, INSERM 1236, Rennes 1 University, 35000 Rennes, France.ORCID 0000-0002-8519-4427
Jean-Claude AldigierImmunology Department, UMR CNRS 7276 INSERM 1262, Limoges University, 87032 Limoges, France.
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

Région Nouvelle-Aquitaine appel d'offre 2017
6 · The paper itself

Abstract

IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world. It was first described in 1968 by Jean Berger and Nicole Hinglais as the presence of intercapillary deposits of IgA. Despite this simple description, patients with IgAN may present very broad clinical features ranging from the isolated presence of IgA in the mesangium without clinical or biological manifestations to rapidly progressive kidney failure. These features are associated with a variety of histological lesions, from the discrete thickening of the mesangial matrix to diffuse cell proliferation. Immunofluorescence on IgAN kidney specimens shows the isolated presence of IgA or its inconsistent association with IgG and complement components. This clinical heterogeneity of IgAN clearly echoes its complex and multifactorial pathophysiology in humans, inviting further analyses of its various aspects through the use of experimental models. Small-animal models of IgAN provide the most pertinent strategies for studying the multifactorial aspects of IgAN pathogenesis and progression. Although only primates have the IgA1 subclass, several murine models have been developed in which various aspects of immune responses are deregulated and which are useful in the understanding of IgAN physiopathology as well as in the assessment of IgAN therapeutic approaches. In this manuscript, we review all murine IgAN models developed since 1968 and discuss their remarkable contribution to understanding the disease.

Indexed as

IgAIgA nephropathykidney mesangiummouse model

Identifiers

PMID34300307
PMCPMC8306110
OpenAlexW3185388285

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.