Evidence map›Paper›PMID 27777266›Full record

ReviewJournal of the American Society of Nephrology : JASN2017

A Proposal for a Serology-Based Approach to Membranous Nephropathy.

An S De Vriese, Richard J Glassock, Karl A Nath, Sanjeev Sethi, Fernando C Fervenza

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
182citing papers in PubMed, 3 pooled it
20.2field-weighted citation impact, top 1% 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

182 citing papers in PubMed, 3 syntheses or guidelines pooled it, 365 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. High-Dose Rituximab and Early Remission in PLA2R1-Related Membranous Nephropathy.Clinical journal of the American Society of Nephrology : CJASN · 2019
    Trial
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
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  14. Review
  15. Article
  16. How to Cure Autoimmune GN and Podocytopathies.Journal of the American Society of Nephrology : JASN · 2026
    Review
  17. Article
  18. Article
  19. Article
  20. Review

122 more citing papers are in PubMed but not listed here.

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

5 authors at 4 institutions in 2 countries.

An S De VrieseDivision of Nephrology, AZ Sint-Jan Brugge-Oostende, Brugge, Belgium; an.devriese@azsintjan.be fervenza.fernando@mayo.edu.
Richard J GlassockDepartment of Medicine, Geffen School of Medicine, University of California, Los Angeles, California; and.
Karl A NathDivision of Nephrology and Hypertension and.
Sanjeev SethiDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota.
Fernando C FervenzaDivision of Nephrology and Hypertension and an.devriese@azsintjan.be fervenza.fernando@mayo.edu.
Hypertension Institute · USAZ Sint-Jan · BEMayo Clinic · USUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary membranous nephropathy (MN) is an autoimmune disease mainly caused by autoantibodies against the recently discovered podocyte antigens: the M-type phospholipase A2 receptor 1 (PLA2R) and thrombospondin type 1 domain-containing 7A (THSD7A). Assays for quantitative assessment of anti-PLA2R antibodies are commercially available, but a semiquantitative test to detect anti-THSD7A antibodies has been only recently developed. The presence or absence of anti-PLA2R and anti-THSD7A antibodies adds important information to clinical and immunopathologic data in discriminating between primary and secondary MN. Levels of anti-PLA2R antibodies and possibly, anti-THSD7A antibodies tightly correlate with disease activity. Low baseline and decreasing anti-PLA2R antibody levels strongly predict spontaneous remission, thus favoring conservative therapy. Conversely, high baseline or increasing anti-PLA2R antibody levels associate with nephrotic syndrome and progressive loss of kidney function, thereby encouraging prompt initiation of immunosuppressive therapy. Serum anti-PLA2R antibody profiles reliably predict response to therapy, and levels at completion of therapy may forecast long-term outcome. Re-emergence of or increase in antibody titers precedes a clinical relapse. Persistence or reappearance of anti-PLA2R antibodies after kidney transplant predicts development of recurrent disease. We propose that an individualized serology-based approach to MN, used to complement and refine the traditional proteinuria-driven approach, will improve the outcome in this disease.

Indexed as

AlgorithmsAutoantibodiesGlomerulonephritis, MembranousHumansKidney TransplantationPrognosisReceptors, Phospholipase A2Serologic TestsAutoantibodiesPLA2R1 protein, humanReceptors, Phospholipase A2clinical nephrologyImmunology and pathologymembranous nephropathyPLA2RTHSD7A

Identifiers

PMID27777266
PMCPMC5280030
OpenAlexW2532400747

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.