Evidence map›Paper›PMID 27351940›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2016

Immunoglobulin A nephropathy: a pathophysiology view.

Rafaela Cabral Gonçalves Fabiano, Sérgio Veloso Brant Pinheiro, Ana Cristina Simões E Silva

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. New strategies and perspectives on managing IgA nephropathy.Clinical and experimental nephrology · 2019
    Review
  12. Article
  13. Article
  14. The association of theInternational journal of clinical and experimental pathology · 2018
    Article
  15. Article
  16. [Clinical and pathological features in IgA nephropathy with IgG deposition in the glomerular mesangial area].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017
    Article
  17. 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

3 authors at 1 institution in 1 country.

Rafaela Cabral Gonçalves FabianoDivision of Nephrology, Clinics Hospital, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Sérgio Veloso Brant PinheiroUnit of Pediatric Nephrology, Department of Pediatrics, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Ana Cristina Simões E SilvaUnit of Pediatric Nephrology, Department of Pediatrics, Faculty of Medicine, Federal University of Minas Gerais, Belo Horizonte, Brazil. acssilva@hotmail.com.ORCID http://orcid.org/0000-0001-9222-3882
Universidade Federal de Minas Gerais · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimIgA nephropathy is one of the leading causes of primary glomerulonephritis worldwide and an important etiology of renal disease in young adults. IgA nephropathy is considered an immune complex-mediated disease.

methodsThis review article summarizes recent evidence on the pathophysiology of IgA nephropathy.

resultsCurrent studies indicate an ordered sequence of multi-hits as fundamental to disease occurrence. Altered glycan structures in the hinge region of the heavy chains of IgA1 molecules act as auto-antigens, potentially triggering the production of glycan-specific autoantibodies. Recognition of novel epitopes by IgA and IgG antibodies leads to the formation of immune complexes galactose deficient-IgA1/anti-glycan IgG or IgA. Immune complexes of IgA combined with FcαRI/CD89 have also been implicated in disease exacerbation. These nephritogenic immune complexes are formed in the circulation and deposited in renal mesangium. Deposited immune complexes ultimately induce glomerular injury, through the release of pro-inflammatory cytokines, secretion of chemokines and the resultant migration of macrophages into the kidney. The TfR1/CD71 receptor has a pivotal role in mesangial cells. New signaling intracellular mechanisms have also been described.

conclusionThe knowledge of the whole pathophysiology of this disease could provide the rational bases for developing novel approaches for diagnosis, for monitoring disease activity, and for disease-specific treatment.

Indexed as

Glomerulonephritis, IGAAnimalsHumansAnti-glycan antibodiesGalactose deficiencyGlomerulonephritisIgA1 glycosylationIgA nephropathy

Identifiers

PMID27351940
OpenAlexW2474469628

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.