Evidence map›Paper›PMID 11943715›Full record

ArticleThe American journal of pathology2002

Antibody response against perlecan and collagen types IV and VI in chronic renal allograft rejection in the rat.

Simone A Joosten, Mieneke G A van Dixhoorn, Maria C Borrias, Hallgrimur Benediktsson, Peter A van Veelen, Cees van Kooten, Leendert C Paul

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Re-Evaluating the Transplant Glomerulopathy Lesion-Beyond Donor-Specific Antibodies.Transplant international : official journal of the European Society for Organ Transplantation · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Transplant glomerulopathy.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
    Review
  11. Article
  12. Review
  13. Article
  14. Role of 6-O-sulfated heparan sulfate in chronic renal fibrosis.The Journal of biological chemistry · 2014
    Article
  15. Article
  16. Article
  17. Review
  18. Late kidney allograft loss: what we know about it, and what we can do about it.Clinical journal of the American Society of Nephrology : CJASN · 2008
    Review
  19. Transplantation proteomics.Pediatric transplantation · 2005
    Review
  20. 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.

Simone A JoostenDepartment of Nephrology, Leiden University Medical Center, Leiden, The Netherlands. s.a.joosten@lumc.nl
Mieneke G A van Dixhoorn
Maria C Borrias
Hallgrimur Benediktsson
Peter A van Veelen
Cees van Kooten
Leendert C Paul
Leiden University Medical Center · NLUniversity of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic rejection is the leading cause of late renal transplant failure. Various structural lesions are observed in grafts undergoing chronic rejection including glomerular basement membrane (GBM) duplications. The well-established Fisher (F344) to Lewis (LEW) rat renal transplant model for chronic rejection was used to assess the presence and role of the humoral immune response against graft antigens during chronic rejection. LEW recipients of F344 allografts develop transplant glomerulopathy and produce IgG1 antibodies directed against F344 GBM preparations that are detectable 3 weeks after transplantation. Glomerular IgG1 deposition was observed that in vitro co-localized with a rabbit anti-rat GBM antiserum in rejecting F344 grafts; elution experiments of isolated glomeruli yielded IgG1 antibodies reactive in vitro with F344 GBM, but not LEW GBM. Prevention of acute rejection by transient treatment of the recipients with cyclosporin A completely abrogated the production of anti-GBM antibodies. Using proteomic techniques we identified the antigens recognized by the LEW posttransplant sera as being the heparan sulfate proteoglycan perlecan and the alpha1 chain of collagen type VI in association with the alpha5 chain of collagen type IV. In conclusion, LEW recipients of F344 kidney grafts produce IgG1 antibodies against donor type perlecan and alpha1(VI)/alpha5(IV) collagen and develop transplant glomerulopathy. These data implicate an important role for the humoral immune response in the development of glomerulopathy during chronic rejection.

Indexed as

Kidney TransplantationAlbuminuriaAnimalsAntibodiesBasement MembraneBlotting, WesternChronic DiseaseCollagen Type IVCollagen Type VIFluorescent Antibody TechniqueGraft RejectionHeparan Sulfate ProteoglycansImmunoglobulin GKidneyKidney DiseasesKidney GlomerulusAntibodiesCollagen Type IVCollagen Type VIHeparan Sulfate ProteoglycansImmunoglobulin Gperlecan

Identifiers

PMID11943715
PMCPMC1867228
OpenAlexW1992746467

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.