Evidence map›Paper›PMID 25409466›Full record

ArticlePloS one2014

The kinetics of glomerular deposition of nephritogenic IgA.

Kenji Yamaji, Yusuke Suzuki, Hitoshi Suzuki, Kenji Satake, Satoshi Horikoshi, Jan Novak, Yasuhiko Tomino

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Glomerular deposition of galactose-deficient IgA1-containing immune complexes via glomerular endothelial cell injuries.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. 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

7 authors at 2 institutions in 2 countries.

Kenji YamajiDivision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Yusuke SuzukiDivision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Hitoshi SuzukiDivision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Kenji SatakeDivision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Satoshi HorikoshiDivision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Jan NovakDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Yasuhiko TominoDivision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Juntendo University · JPUniversity of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Whether IgA nephropathy is attributable to mesangial IgA is unclear as there is no correlation between intensity of deposits and extent of glomerular injury and no clear mechanism explaining how these mesangial deposits induce hematuria and subsequent proteinuria. This hinders the development of a specific therapy. Thus, precise events during deposition still remain clinical challenge to clarify. Since no study assessed induction of IgA nephropathy by nephritogenic IgA, we analyzed sequential events involving nephritogenic IgA from IgA nephropathy-prone mice by real-time imaging systems. Immunofluorescence and electron microscopy showed that serum IgA from susceptible mice had strong affinity to mesangial, subepithelial, and subendothelial lesions, with effacement/actin aggregation in podocytes and arcade formation in endothelial cells. The deposits disappeared 24-h after single IgA injection. The data were supported by a fluorescence molecular tomography system and real-time and 3D in vivo imaging. In vivo imaging showed that IgA from the susceptible mice began depositing along the glomerular capillary from 1 min and accumulated until 2-h on the first stick in a focal and segmental manner. The findings indicate that glomerular IgA depositions in IgAN may be expressed under the balance between deposition and clearance. Since nephritogenic IgA showed mesangial as well as focal and segmental deposition along the capillary with acute cellular activation, all glomerular cellular elements are a plausible target for injury such as hematuria.

Indexed as

AnimalsBone Marrow TransplantationFemaleFluorescent Antibody TechniqueGlomerular MesangiumGlomerulonephritis, IGAHumansImmunoglobulin AMiceMice, Inbred BALB CMicroscopy, ElectronProteinuriaImmunoglobulin A

Identifiers

PMID25409466
PMCPMC4237359
OpenAlexW2000115445

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.