ReviewSeminars in nephrology2013
The role of complement in membranous nephropathy.
Review in Seminars in nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
99 citing papers in PubMed, 1 synthesis or guideline pooled it, 178 citations in OpenAlex.
- IgG4 anti-phospholipase A2 receptor might activate lectin and alternative complement pathway meanwhile in idiopathic membranous nephropathy: an inspiration from a cross-sectional study.Immunologic research · 2016Pooled it
- The correlation of anti-β2-glycoprotein I antibody with complement activation in patients with idiopathic membranous nephropathy.International urology and nephrology · 2021Trial
- Distinct Complement Activation Profiles Between NELL1- and PLA2R-Associated Membranous Nephropathy: A Clinicopathological and Proteomic Study.Nephrology (Carlton, Vic.) · 2026Article
- Optimization of a Target Antigen Diagnostic Pathway for Membranous Nephropathy.Kidney international reports · 2026Article
- Autoantibodies reactive with glomerular endothelial cells and podocytes in patients with membranous nephropathy.Journal of translational autoimmunity · 2026Article
- Complement Profiling in Glomerular Disease: Insights from Laser Microdissection and Mass Spectrometry.Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- A noninvasive method of diagnosing membranous nephropathy using exosomes derived from urine.Kidney research and clinical practice · 2026Article
- Membranous Nephropathy: Antigenic Landscape and a Novel Pathogenetic Model.International journal of molecular sciences · 2026Review
- Complement role in kidney disease: a comprehensive review and therapeutic innovations.BMC nephrology · 2026Review
- Hyperlipidemia in membranous nephropathy.Clinical kidney journal · 2026Review
- Not So Benign: Revisiting Pure Membranous Lupus Nephritis.Journal of personalized medicine · 2025Review
- Review
- Intercepting the complement amplification loop through podocyte MC5R signaling ameliorates membranous nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Identification of potential therapeutic targets for complement-associated glomerular diseases using Mendelian randomization.Medicine · 2025Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Chronic kidney disease enhances alternative pathway activity: a new paradigm.The Journal of clinical investigation · 2025Review
- Urine complement analysis implies complement activation is involved in membranous nephropathy.Frontiers in medicine · 2025Article
- [What is proven in the treatment of complement-mediated kidney diseases?]Innere Medizin (Heidelberg, Germany) · 2024Review
- [The complement cascade in renal pathology].Pathologie (Heidelberg, Germany) · 2024Review
- Dissociation Phenomenon of Erythrocyte Agglutination and Its Application to Assay of Functional Activity of the Complement System in Clinical Laboratory.Journal of clinical laboratory analysis · 2024Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Membranous nephropathy (MN) describes a histopathologic pattern of injury marked by glomerular subepithelial immune deposits and collectively represents one of the most common causes of adult nephrotic syndrome. Studies in Heymann nephritis, an experimental model of MN, have established a paradigm in which these deposits locally activate complement to cause podocyte injury, culminating in cytoskeletal reorganization, loss of slit diaphragms, and proteinuria. There is much circumstantial evidence for a prominent role of complement in human MN because C3 and C5b-9 are found consistently within immune deposits. Secondary MN often shows the additional presence of C1q, implicating the classic pathway of complement activation. Primary MN, however, is IgG4-predominant and IgG4 is considered incapable of binding C1q and activating the complement pathway. Recent studies have identified the M-type phospholipase A2 receptor (PLA2R) as the major target antigen in primary MN. Early evidence hints that IgG4 anti-PLA2R autoantibodies can bind mannan-binding lectin and activate the lectin complement pathway. The identification of anti-PLA2R antibodies as likely participants in the pathogenesis of disease will allow focused investigation into the role of complement in MN. Definitive therapy for MN is immunosuppression, although future therapeutic agents that specifically target complement activation may represent an effective temporizing measure to forestall further glomerular injury.
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Registered trials
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.