Evidence map›Paper›PMID 37090184›Full record

ArticleGlomerular diseases

A Genetic Risk Score Distinguishes Different Types of Autoantibody-Mediated Membranous Nephropathy.

Sanjana Gupta, Mallory Lorraine Downie, Chris Cheshire, Stephanie Dufek-Kamperis, Adam Paul Levine, Paul Brenchley, Elion Hoxha, Rolf Stahl, Neil Ashman, Ruth Jennifer Pepper and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Glomerular diseases. 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
0.8field-weighted citation impact, top 30% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

16 authors at 5 institutions in 2 countries.

Sanjana GuptaUCL Department of Renal Medicine, University College London, London, UK.
Mallory Lorraine DownieUCL Department of Renal Medicine, University College London, London, UK.
Chris CheshireUCL Department of Renal Medicine, University College London, London, UK.
Stephanie Dufek-KamperisUCL Department of Renal Medicine, University College London, London, UK.
Adam Paul LevineUCL Department of Renal Medicine, University College London, London, UK.
Paul BrenchleyInstitute of Cardiovascular Sciences, University of Manchester, Manchester, UK.
Elion HoxhaDepartment of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Rolf StahlDepartment of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Neil AshmanDepartment of Renal Medicine, Barts Health, London, UK.
Ruth Jennifer PepperUCL Department of Renal Medicine, University College London, London, UK.
Sean MasonUCB Pharma, Slough, UK.
Jill NormanUCL Department of Renal Medicine, University College London, London, UK.
Detlef BockenhauerUCL Department of Renal Medicine, University College London, London, UK.
Horia Constantin StanescuUCL Department of Renal Medicine, University College London, London, UK.
Robert KletaUCL Department of Renal Medicine, University College London, London, UK.
Daniel Philip GaleUCL Department of Renal Medicine, University College London, London, UK.
University College London · GBUniversität Hamburg · DEBarts Health NHS Trust · GBUCB Pharma (United Kingdom) · GBUniversity of Manchester · GB

Funding

Medical Research Council MR/J010847/1
6 · The paper itself

Abstract

Introduction: Membranous nephropathy (MN) is the leading cause of nephrotic syndrome in adults and is characterized by detectable autoantibodies against glomerular antigens, most commonly phospholipase A2 receptor 1 (PLA2R1) and thrombospondin type-1 domain containing 7A (THSD7A). In Europeans, genetic variation in at least five loci, Methods: 1,409 MN individuals were genotyped genome-wide with a dense SNV array. The genetic risk score (GRS) was calculated utilizing the previously identified European MN loci, and results were compared with 4,929 healthy controls and 422 individuals with steroid-sensitive nephrotic syndrome. Results: GRS was calculated in the 759 MN individuals in whom antibody status was known. The GRS for MN was elevated in the anti-PLA2R1 antibody-positive ( Conclusion: We demonstrate that the genetic risk factors for PLA2R1- and THSD7A-antibody-associated MN are different. A higher GRS is associated with younger age of onset of disease. Further, a proportion of antibody-negative MN cases have an elevated GRS similar to PLA2R1-positive disease. This suggests that in some individuals with negative serology the disease is driven by autoimmunity against PLA2R1.

Indexed as

AutoantibodyGenetic risk scoreMembranous nephropathyPhospholipase A2 receptor 1Thrombospondin type-1 domain containing 7A

Identifiers

PMID37090184
PMCPMC10116192
OpenAlexW4323034275

What OpenQuestion holds

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LicenceCC BY-NC
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.