Evidence map›Paper›PMID 25722731›Full record

ArticleDrug discovery today. Disease models2014

Development of Animal Models of Human IgA Nephropathy.

Hitoshi Suzuki, Yusuke Suzuki, Jan Novak, Yasuhiko Tomino

Abstract read
In one paragraph

Article in Drug discovery today. Disease models, 2014. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Autoimmune-mediated renal disease and hypertension.Clinical science (London, England : 1979) · 2021
    Review
  8. Article
  9. Role of Polymeric Immunoglobulin Receptor in IgA and IgM Transcytosis.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Article
  12. Nephroprotective effect of losartan in IgA model rat.The Journal of international medical research · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Primary IgA nephropathy: current challenges and future prospects.International journal of nephrology and renovascular disease · 2018
    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

4 authors.

Hitoshi SuzukiDivision of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine, Tokyo, Japan.
Yusuke SuzukiDivision of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine, Tokyo, Japan.
Jan NovakDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA.
Yasuhiko TominoDivision of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine, Tokyo, Japan.

Funding

Elucidating IgA Nephropathy through Genetic Studies of IgA1 GlycosylationR01DK082753 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GHARAVI, ALI G, NOVAK, JAN · 2009 to 2024
$8.7M
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR01DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JAN NOVAK · 2007 to 2026
$6.0M
Analytical tools for the analysis of clustered O-glycans in clinical samplesR01GM098539 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RENFROW, MATTHEW B · 2011 to 2019
$2.7M
Molecular Basis of Pathogenicity of IgA1-containing Immune ComplexesR56DK078244 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NOVAK, JAN · 2012 to 2012
$92k
NIDDK NIH HHS R01 DK078244NIDDK NIH HHS R01 DK082753NIDDK NIH HHS R56 DK078244NIGMS NIH HHS R01 GM098539
6 · The paper itself

Abstract

IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis in the world. IgAN is characterized by the mesangial accumulation of immune complexes containing IgA1, usually with co-deposits of complement C3 and variable IgG and/or IgM. Although more than 40 years have passed since IgAN was first described, the mechanisms underlying the disease development are not fully understood. Small-animal experimental models of IgAN can be very helpful in studies of IgAN, but development of these models has been hindered by the fact that only humans and hominoid primates have IgA1 subclass. Thus, multiple models have been developed, that may be helpful in studies of some specific aspects of IgAN. These models include a spontaneous animal model of IgAN, the ddY mouse first reported in 1985. These mice show mild proteinuria without hematuria, and glomerular IgA deposits, with a highly variable incidence and degree of glomerular injury, due to the heterogeneous genetic background. To obtain a murine line consistently developing IgAN, we intercrossed an earlyonset group of ddY mice, in which the development of IgAN includes mesangial IgA deposits and glomerular injury. After selective intercrossing for >20 generations, we established a novel 100% early-onset grouped ddY murine model. All grouped ddY mice develop proteinuria within eight weeks of age. The grouped ddY mouse model can be a useful tool for analysis of multiple aspects of the pathogenesis of IgAN and may aid in assessment of some approaches for the treatment of IgAN.

Identifiers

PMID25722731
PMCPMC4337240

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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.