Evidence map›Paper›PMID 24741606›Full record

ReviewJournal of immunology research2014

Transplant glomerulopathy: the interaction of HLA antibodies and endothelium.

William Hanf, Claudine S Bonder, P Toby H Coates

Open access · goldAbstract readReview
In one paragraph

Review in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 33 citations in OpenAlex.

  1. Re-Evaluating the Transplant Glomerulopathy Lesion-Beyond Donor-Specific Antibodies.Transplant international : official journal of the European Society for Organ Transplantation · 2024
    Review
  2. The five types of glomerulonephritis classified by pathogenesis, activity and chronicity (GN-AC).Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Article
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  12. Renal allograft rejection: pieces of the puzzle.Journal of the American Society of Nephrology : JASN · 2015
    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

3 authors at 2 institutions in 1 country.

William HanfCentral Northern Adelaide Renal & Transplantation Service, Royal Adelaide Hospital, Adelaide, SA 5000, Australia.
Claudine S BonderCentre for Cancer Biology, SA Pathology, Frome Road, Adelaide, SA 5000, Australia ; Department of Medicine, University of Adelaide, Frome Road, Adelaide, SA 5000, Australia ; Centre for Stem Cell Research, University of Adelaide, Frome Road, Adelaide, SA 5000, Australia.
P Toby H CoatesCentral Northern Adelaide Renal & Transplantation Service, Royal Adelaide Hospital, Adelaide, SA 5000, Australia ; Department of Medicine, University of Adelaide, Frome Road, Adelaide, SA 5000, Australia ; Centre for Stem Cell Research, University of Adelaide, Frome Road, Adelaide, SA 5000, Australia ; Clinical and Experimental Transplantation Group, Royal Adelaide Hospital, North Terrace, Adelaide, SA 5000, Australia.
University of Adelaide · AURoyal Adelaide Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transplant glomerulopathy (TG) is a major cause of chronic graft dysfunction without effective therapy. Although the histological definition of TG is well characterized, the pathophysiological pathways leading to TG development are still poorly understood. Electron microscopy suggests an earlier appearance of TG and suggests that endothelial cell injury is the first sign of the disease. The pathogenic role of human leukocyte antigen (HLA) antibodies in endothelial cells has been described in acute vascular and humoral rejection. However the mechanisms and pathways of endothelial cell injury by HLA antibodies remain unclear. Despite the description of different causes of the morphological lesion of TG (hepatitis, thrombotic microangiopathy), the strong link between TG and chronic antibody mediated rejection suggests a major role for HLA antibodies in TG formation. In this review, we describe the effect of classes I or II HLA-antibodies in TG and especially the implication of donor specific antibodies (DSA). We update recent studies about endothelial cells and try to explain the different signals and intracellular pathways involved in the progression of TG.

Indexed as

Antibody SpecificityAutoantibodiesComplement C4EndotheliumGlomerulonephritisHLA AntigensHumansPatient Outcome AssessmentRisk FactorsTransplantsAutoantibodiesComplement C4HLA Antigens

Identifiers

PMID24741606
PMCPMC3987972
OpenAlexW1984826837

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.