ArticleJournal of the American Society of Nephrology : JASN2016
Phospholipase A2 Receptor-Related Membranous Nephropathy and Mannan-Binding Lectin Deficiency.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Recent Advances in Clinical Diagnosis and Pharmacotherapy Options of Membranous Nephropathy.Frontiers in pharmacology · 2022Pooled it
- Biomarkers in the Management of Complement-Mediated Kidney Diseases in the Era of Complement Therapeutics.Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- Complement role in kidney disease: a comprehensive review and therapeutic innovations.BMC nephrology · 2026Review
- Treatment strategies for rituximab-resistant primary membranous nephropathy: from resistance mechanisms to emerging therapies.Frontiers in immunology · 2026Review
- Clinical evaluation of strengthening spleen and draining dampness in the treatment of idiopathic membranous nephropathy: a retrospective 10-year follow-up study.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Complement System Inhibitors in Nephrology: An Update-Narrative Review.International journal of molecular sciences · 2025Review
- Complement Activation in Nephrotic Glomerular Diseases.Biomedicines · 2024Review
- Novel biomarkers and pathophysiology of membranous nephropathy: PLA2R and beyond.Clinical kidney journal · 2024Review
- Urinary complement biomarkers in immune-mediated kidney diseases.Frontiers in immunology · 2024Review
- The role of complement in kidney disease.Nature reviews. Nephrology · 2023Review
- Towards the Definition of the Molecular Hallmarks of Idiopathic Membranous Nephropathy in Serum Proteome: A DIA-PASEF Approach.International journal of molecular sciences · 2023Article
- Glomerulonephritis: immunopathogenesis and immunotherapy.Nature reviews. Immunology · 2023Review
- The classical pathway triggers pathogenic complement activation in membranous nephropathy.Nature communications · 2023Article
- Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.Frontiers in immunology · 2023Review
- Kidney diseases.Immunological reviews · 2023Review
- Lectin Complement Pathway Activation is Associated with Massive Proteinuria in PLA2R-Positive Membranous Nephropathy: A Retrospective Study.International journal of general medicine · 2023Article
- Factors affecting IgG4-mediated complement activation.Frontiers in immunology · 2023Article
- Observational
- The Rational Use of Complement Inhibitors in Kidney Diseases.Kidney international reports · 2022Review
- Definition of IgG Subclass-Specific Glycopatterns in Idiopathic Membranous Nephropathy: Aberrant IgG Glycoforms in Blood.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Most patients with idiopathic membranous nephropathy (IMN) have IgG4 autoantibodies against phospholipase A2 receptor (PLA2R). C3 and C5b-9 are found in immune deposits of IMN kidney biopsy specimens, but the pathway of complement activation in IMN remains elusive. We report the case of a patient who developed IMN with intense staining for PLA2R, IgG4, C3, C5b-9, factor B, and properdin and very weak staining for C1q, C4d, and IgG1. Measurement of mannan binding lectin (MBL) antigenic level and activity revealed MBL deficiency. Genotyping revealed a heterozygous (A/C) polymorphism in codon 57 of MBL2 exon 1 associated with homozygous and heterozygous variations in the promoter region at -550 (L/L) and -221 (X/Y), respectively, suggesting that the patient harbored the LXA/LYC haplotypes linked to MBL deficiency. Genetic sequencing in 77 consecutive patients with IMN identified four patients with MBL2 promoter and coding region variations associated with MBL deficiency and the same complement pattern in immune deposits as the index patient. In contrast, patients with wild-type MBL2 had immune deposits with intense Cd4 staining. Thus, IMN can develop in patients with complete MBL deficiency, with complement activated mainly by the alternative pathway, whereas the lectin pathway is also activated in those with wild-type MBL2.
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Registered trials
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