Evidence map›Paper›PMID 32195325›Full record

ArticleTransplantation direct2020

High-activity Classical and Alternative Complement Pathway Genotypes-Association With Donor-specific Antibody-triggered Injury and Renal Allograft Survival.

Blanka Mező, Roman Reindl-Schwaighofer, Farsad Eskandary, Andreas Heinzel, Markus Wahrmann, Konstantin Doberer, Andreas Heilos, Gregor Bond, Johannes Kläger, Nicolas Kozakowski and 8 more

Abstract read
In one paragraph

Article in Transplantation direct, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Observational
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

18 authors.

Blanka MezőResearch Laboratory, IIIrd Department of Internal Medicine and MTA-SE Research Group of Immunology and Hematology, Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary.
Roman Reindl-SchwaighoferDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Farsad EskandaryDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Andreas HeinzelDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Markus WahrmannDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Konstantin DobererDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Andreas HeilosDepartment of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.
Gregor BondDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Johannes KlägerDepartment of Pathology, Medical University of Vienna, Vienna, Austria.
Nicolas KozakowskiDepartment of Pathology, Medical University of Vienna, Vienna, Austria.
Helmuth HaslacherDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Rainer OberbauerDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.
Ondřej ViklickýDepartment of Nephrology, Transplant Center, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
Petra HrubáDepartment of Nephrology, Transplant Center, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
Philip F HalloranAlberta Transplant Applied Genomics Centre, ATAGC, University of Alberta, Edmonton, AB, Canada.
Krisztina RusaiDepartment of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.
Zoltán ProhászkaResearch Laboratory, IIIrd Department of Internal Medicine and MTA-SE Research Group of Immunology and Hematology, Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary.
Georg A BöhmigDepartment of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundComplement may contribute to donor-specific antibody (DSA)-triggered transplant injury. Here, we investigated whether the intrinsic strength of classical pathway and alternative pathway (AP) relates to the pathogenicity of DSA.

methodsClassical pathway and AP high-activity genotypes were defined according to C4 gene copy number and the presence of functional polymorphisms in C3 (C3

resultsIn the cohort of DSA-positive subjects, the number of C4 gene copies was related to C4 protein levels in serum and capillary C4d staining, but not AMR activity. Patients with a high-activity AP complotype, which was associated with complement consumption in serum, showed enhanced microcirculation inflammation (median glomerulitis plus peritubular capillaritis score, 2 [interquartile range, 0-4 versus 1 0-2];

conclusionsOur study suggests a contribution of complement genetics to the phenotypic presentation of AMR. Future studies will have to clarify whether a possible association of AP strength with graft survival relates to enhanced antibody-triggered injury.

Identifiers

PMID32195325
PMCPMC7056277

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