Evidence map›Paper›PMID 9763614›Full record

ArticleThe Journal of experimental medicine1998

Inhibition of complement regulation is key to the pathogenesis of active Heymann nephritis.

B Schiller, C He, D J Salant, A Lim, J J Alexander, R J Quigg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Unmet challenges in membranous nephropathy.Current opinion in nephrology and hypertension · 2019
    Review
  5. Article
  6. Article
  7. Review
  8. Membranous nephropathy: from models to man.The Journal of clinical investigation · 2014
    Review
  9. Review
  10. Review
  11. Article
  12. Experimental membranous nephropathy redux.American journal of physiology. Renal physiology · 2005
    Review
  13. Review
  14. Complement regulation during pregnancy.Immunologic research · 2005
    Review
  15. Article
  16. Article
  17. Production of a new model of slowly progressive Heymann nephritis.International journal of experimental pathology · 2003
    Article
  18. 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

6 authors at 2 institutions in 1 country.

B SchillerDepartment of Medicine, Section of Nephrology, The University of Chicago, Chicago, Illinois 60637, USA.
C He
D J Salant
A Lim
J J Alexander
R J Quigg
University Medical Center · USBoston University · US

Funding

MEDIATION OF ANTIBODY-INDUCED GLOMERULAR INJURYR01DK030932 · NIDDK · BOSTON UNIVERSITY MEDICAL CENTER HOSP · PI SALANT, DAVID J · 1986 to 2010
$3.4M
Role of the Complement System in Renal DiseaseR01DK041873 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI QUIGG, RICHARD J. · 1994 to 2011
$3.4M
Nephrology Research Training GrantT32DK007510 · NIDDK · UNIVERSITY OF CHICAGO · PI COE, FREDERIC L · 1986 to 2013
$2.1M
Antibody Mediated Glomerular InjuryR56DK030932 · NIDDK · BOSTON MEDICAL CENTER · PI SALANT, DAVID J · 2005 to 2005
$81k
Role of the complement system in renal diseaseR56DK041873 · NIDDK · UNIVERSITY OF CHICAGO · PI QUIGG, RICHARD J · 2006 to 2006
$75k
COMPLEMENT ACTIVATION OF THE GLOMERULER EPITHELIAL CELLR29DK041873 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI QUIGG, RICHARD J · 1989 to 1993
–
NIDDK NIH HHS DK07510NIDDK NIH HHS DK30932NIDDK NIH HHS DK41873NIDDK NIH HHS R01 DK030932NIDDK NIH HHS R01 DK041873NIDDK NIH HHS R56 DK030932NIDDK NIH HHS R56 DK041873NIDDK NIH HHS T32 DK007510
6 · The paper itself

Abstract

Crry (complement receptor 1-related protein/gene y) is a key cellular complement regulator in rodents. It is also present in Fx1A, the renal tubular preparation used to immunize rats to induce active Heymann nephritis (HN), a model of membranous nephropathy. We hypothesized that rats immunized with anti-Fx1A develop autoantibodies (auto-Abs) to Crry as well as to the megalin-containing HN antigenic complex, and that anti-Crry Abs promote the development of injury in HN by neutralizing the complement regulatory activity of Crry. Rats immunized with Fx1A lacking Crry remained free of proteinuria and glomerular deposits of C3 during a 10-wk follow-up despite typical granular immunoglobulin (Ig)G deposits in glomeruli. Anti-Fx1A auto-Abs were present in their sera at levels that were not different from sera pooled from proteinuric rats with HN induced with nephritogenic Fx1A. Passive administration of sheep anti-Crry Abs to rats immunized with Crry-deficient Fx1A led to proteinuria and glomerular C3 deposition, which were not seen in such rats injected with preimmune IgG, nor in rats with collagen-induced arthritis injected with anti-Crry IgG. To directly examine the role of Crry in HN, rats were immunized with Crry-deficient Fx1A reconstituted with rCrry. This led to typical HN, with 8 out of 15 rats developing proteinuria within 14 wk. Moreover, the extent of glomerular C3 deposition correlated with proteinuria, and anti-Crry Abs were present in glomerular eluates. Thus, Crry is a key nephritogenic immunogen in Fx1A. Formation of neutralizing auto-Abs to Crry impairs its function, leading to unrestricted complement activation by Abs reactive with the HN antigenic complex on the epithelial cell surface.

Indexed as

AnimalsAntigens, SurfaceComplement System ProteinsFemaleGlomerulonephritisRatsRats, Inbred LewRats, Sprague-DawleyReceptors, Cell SurfaceReceptors, ComplementAntigens, SurfaceComplement System ProteinsCr1l protein, ratReceptors, Cell SurfaceReceptors, Complement

Identifiers

PMID9763614
PMCPMC2212493
OpenAlexW2079820146

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.