ArticleJournal of the American Society of Nephrology : JASN2020
Large-Scale Whole-Genome Sequencing Reveals the Genetic Architecture of Primary Membranoproliferative GN and C3 Glomerulopathy.
Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Systematic review of associations between HLA and renal function.International journal of immunogenetics · 2022Pooled it
- From data to drug: the translational impact of RaDaR, the UK national registry of rare kidney diseases.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026Review
- The Genomic Infinity Loop.Journal of the American Society of Nephrology : JASN · 2026Article
- Real-World Patient Characteristics, Burden, and Quality of Life in C3 Glomerulopathy and Primary Immune Complex Membranoproliferative GN.Kidney360 · 2026Article
- Recurrence of C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis After Kidney Transplantation: Challenges and Opportunities.Kidney international reports · 2026Review
- Current and Emerging Therapies for C3 Glomerulopathy and Primary (Idiopathic) Immune Complex Membranoproliferative Glomerulonephritis.Kidney international reports · 2026Review
- Article
- Primary membranoproliferative glomerulonephritis: natural history, pathogenesis, and treatment.Frontiers in nephrology · 2026Review
- Kidney transplant in patients with C3 glomerulopathy.Clinical kidney journal · 2025Review
- Acquired drivers of C3 glomerulopathy.Clinical kidney journal · 2025Review
- Challenges in the Diagnosis and Management of Immune Complex-Mediated Membranoproliferative Glomerulonephritis and Complement 3 Glomerulopathy.Kidney international reports · 2025Review
- Morphological and etiological analyses of C3 and non-C3 glomerulonephritis in primary membranoproliferative glomerulonephritis using periodic acid-methenamine silver stain electron microscopy: a retrospective multicentered study.Medical molecular morphology · 2024Article
- The Association of Class I and II Human Leukocyte Antigen Serotypes With End-Stage Kidney Disease Due to Membranoproliferative Glomerulonephritis and Dense Deposit Disease.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2024Article
- Nephritis-Associated Plasmin Receptor (NAPlr): An Essential Inducer of C3-Dominant Glomerular Injury and a Potential Key Diagnostic Biomarker of Infection-Related Glomerulonephritis (IRGN).International journal of molecular sciences · 2022Review
- Rare complement factor I variants associated with reduced macular thickness and age-related macular degeneration in the UK Biobank.Human molecular genetics · 2022Article
- Emerging Role of Clinical Genetics in CKD.Kidney medicine · 2022Review
- Long-term follow-up including extensive complement analysis of a pediatric C3 glomerulopathy cohort.Pediatric nephrology (Berlin, Germany) · 2022Article
- A clinical approach to children with C3 glomerulopathy.Pediatric nephrology (Berlin, Germany) · 2022Review
- Challenges in diagnostic testing of nephritic factors.Frontiers in immunology · 2022Review
- Characteristics and outcomes of glomerulonephritis with membranoproliferative pattern in children.Translational pediatrics · 2021Article
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Authors and funding
25 authors at 10 institutions in 1 country.
Funding
Abstract
backgroundPrimary membranoproliferative GN, including complement 3 (C3) glomerulopathy, is a rare, untreatable kidney disease characterized by glomerular complement deposition. Complement gene mutations can cause familial C3 glomerulopathy, and studies have reported rare variants in complement genes in nonfamilial primary membranoproliferative GN.
methodsWe analyzed whole-genome sequence data from 165 primary membranoproliferative GN cases and 10,250 individuals without the condition (controls) as part of the National Institutes of Health Research BioResource-Rare Diseases Study. We examined copy number, rare, and common variants.
resultsOur analysis included 146 primary membranoproliferative GN cases and 6442 controls who were unrelated and of European ancestry. We observed no significant enrichment of rare variants in candidate genes (genes encoding components of the complement alternative pathway and other genes associated with the related disease atypical hemolytic uremic syndrome; 6.8% in cases versus 5.9% in controls) or exome-wide. However, a significant common variant locus was identified at 6p21.32 (rs35406322) (
conclusionsWe found that HLA type, but not rare complement gene variation, is associated with primary membranoproliferative GN. These findings challenge the paradigm of complement gene mutations typically causing primary membranoproliferative GN and implicate an underlying autoimmune mechanism in most cases.
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