Evidence map›Paper›PMID 33042109›Full record

ReviewFrontiers in immunology2020

Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity.

Wenbin Liu, Chang Gao, Zhiyuan Liu, Haoran Dai, Zhendong Feng, Zhaocheng Dong, Yang Zheng, Yu Gao, Xuefei Tian, Baoli Liu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
4.6field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. NELL-1: role and mechanisms in disease pathogenesis and development.Frontiers in cell and developmental biology · 2026
    Review
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  20. Kynurenine pathway in kidney diseases.Pharmacological reports : PR · 2022
    Review
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

10 authors at 5 institutions in 2 countries.

Wenbin LiuBeijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
Chang GaoBeijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
Zhiyuan LiuBasic Medical College, Taishan Medical University, Tai'an, China.
Haoran DaiBeijing Chinese Medicine Hospital PingGu Hospital, Beijing, China.
Zhendong FengShunyi Branch, Beijing Hospital of Traditional Chinese Medicine, Beijing, China.
Zhaocheng DongBeijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
Yang ZhengBeijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
Yu GaoBeijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
Xuefei TianSection of Nephrology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United States.
Baoli LiuBeijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
Beijing Hospital of Traditional Chinese Medicine · CNCapital Medical University · CNShunyi Hospital of Beijing Traditional Chinese Medicine Hospital · CNTaishan Medical University · CNYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic membranous nephropathy (IMN) is a pathological pattern of glomerular damage caused by an autoimmune response. Immune complex deposition, thickness of glomerular basement membrane, and changes in the podocyte morphology are responsible for the development of proteinuria, which is caused by the targeted binding of auto-antibodies to podocytes. Several auto-antigens have recently been identified in IMN, including M-type receptor for secretory phospholipase A2 (PLA2R1), thrombospondin type-1 domain-containing 7A (THSD7A), and neural epidermal growth factor-like 1 protein (NELL-1). The measurement of peripheral circulating antibodies has become an important clinical reference index. However, some clinical features of IMN remain elusive and need to be further investigated, such as the autoimmunity initiation, IgG4 predominance, spontaneous remission, and the unique glomerular lesion. As these unresolved issues are closely related to clinical practice, we have proposed a hypothetical pathogenesis model of IMN. Induced by environmental stimuli or other causes, the PLA2R1 antigen and/or THSD7A antigen exposed to extrarenal tissues, such as lungs, then produce the auto-antibodies that target and cause damage to the podocytes in circulation. In this review, we highlighted the potential association between environmental stimuli, immune activity, and glomerular lesions, the underlying basis for spontaneous immune and proteinuria remission.

Indexed as

Models, ImmunologicalAutoantibodiesAutoantigensGlomerulonephritis, MembranousHumansPodocytesAutoantibodiesAutoantigensautoimmune responseenvironmental stimuliinflammationpathogenesis modelpodocytespontaneous remission

Identifiers

PMID33042109
PMCPMC7524879
OpenAlexW3085757443

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.