Evidence map›Paper›PMID 39941432›Full record

ReviewJournal of clinical medicine2025

Membranous Nephropathy.

Claudio Ponticelli

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. [Nephrotic syndrome].Innere Medizin (Heidelberg, Germany) · 2025
    Review
  9. Article
  10. 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

1 author.

Claudio PonticelliIndependent Researcher, 20131 Milano, Italy.ORCID 0000-0001-6060-965X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Membranous nephropathy is a glomerular disease that may be caused by exogenous risk factors in genetically predisposed individuals (primary MN) or may be associated with other autoimmune diseases, drug exposure, or cytotoxic agents (secondary MN). Primary membranous nephropathy (PMN) is an autoimmune disease in which antigens-mainly the phospholipase A2 receptor-are located in the podocytes and are targeted by circulating antibodies, leading to in situ formation of immune complexes that activate the complement system. Clinically, the disease is characterized by nephrotic syndrome (NS) and associated complications. The outcome of PMN can vary, but untreated patients with NS may progress to end-stage kidney disease (ESKD) in 35-40% of cases within 10 years. Treatment primarily aims to prevent NS complications and progression to ESKD. The most commonly used immunosuppressive drugs are rituximab, corticosteroids, cyclophosphamide, and calcineurin inhibitors. Most patients may experience an improvement of proteinuria, which can sometimes be followed by NS relapse. Fewer than 50% of patients with PMN achieve complete and stable remission. In addition to immunosuppressive therapy, antiproteinuric, anti-lipemic, and anticoagulant medicaments are often required.

Indexed as

glomerulonephritismembranous nephropathynephrotic syndromepodocyteproteinuria

Identifiers

PMID39941432
PMCPMC11818350

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.