Evidence map›Paper›PMID 28550082›Full record

ReviewClinical journal of the American Society of Nephrology : CJASN2017

Primary Membranous Nephropathy.

William G Couser

Erratum issuedOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical journal of the American Society of Nephrology : CJASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 382 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
382citing papers in PubMed, 3 pooled it
27.3field-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

382 citing papers in PubMed, 3 syntheses or guidelines pooled it, 653 citations in OpenAlex.

  1. Pooled it
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  5. Observational
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  20. Membranous Nephropathy: Antigenic Landscape and a Novel Pathogenetic Model.International journal of molecular sciences · 2026
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

William G CouserDivision of Nephrology, Department of Medicine, University of Washington, Seattle, Washington.
University of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Membranous nephropathy (MN) is a unique glomerular lesion that is the most common cause of idiopathic nephrotic syndrome in nondiabetic white adults. About 80% of cases are renal limited (primary MN, PMN) and 20% are associated with other systemic diseases or exposures (secondary MN). This review focuses only on PMN. Most cases of PMN have circulating IgG4 autoantibody to the podocyte membrane antigen PLA2R (70%), biopsy evidence PLA2R staining indicating recent immunologic disease activity despite negative serum antibody levels (15%), or serum anti-THSD7A (3%-5%). The remaining 10% without demonstrable anti-PLA2R/THSd7A antibody or antigen likely have PMN probably secondary to a different, still unidentified, anti-podocyte antibody. Considerable clinical and experimental data now suggests these antibodies are pathogenic. Clinically, 80% of patients with PMN present with nephrotic syndrome and 20% with non-nephrotic proteinuria. Untreated, about one third undergo spontaneous remission, especially those with absent or low anti-PLA2R levels, one-third progress to ESRD over 10 years, and the remainder develop nonprogressive CKD. Proteinuria can persist for months after circulating anti-PLA2R/THSD7A antibody is no longer detectable (immunologic remission). All patients with PMN should be treated with supportive care from the time of diagnosis to minimize protein excretion. Patients with elevated anti-PLA2R/THSD7A levels and proteinuria >3.5 g/d at diagnosis, and those who fail to reduce proteinuria to <3.5 g after 6 months of supportive care or have complications of nephrotic syndrome, should be considered for immunosuppressive therapy. Accepted regimens include steroids/cyclophosphamide, calcineurin inhibitors, and B cell depletion. With proper management, only 10% or less will develop ESRD over the subsequent 10 years.

Indexed as

Glomerulonephritis, MembranousKidneyAutoantibodiesBiomarkersDisease ProgressionHumansImmunoglobulin GImmunosuppressive AgentsReceptors, Phospholipase A2Remission InductionRisk FactorsThrombospondinsTime FactorsTreatment OutcomeAutoantibodiesBiomarkersImmunoglobulin GImmunosuppressive AgentsReceptors, Phospholipase A2ThrombospondinsTHSD7A protein, humanAdultBiopsyB-LymphocytesCalcineurin InhibitorsChroniccongenitalCyclophosphamideGlomerulonephritishumanHumansImmunoglobulin GKidney FailureKidney GlomerulusLipoidMembranousmembranous nephropathyNephrosisnephrotic syndromePhospholipase A2PLA2RPLA2R1 proteinPodocytesproteinuriaReceptorsRemissionRenal InsufficiencySpontaneousStaining and LabelingTHSD7A

Identifiers

PMID28550082
PMCPMC5460716
OpenAlexW2617482626

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.