ArticleKidney international2009
Glomeruli of Dense Deposit Disease contain components of the alternative and terminal complement pathway.
Article in Kidney international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.
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Who cites it
96 citing papers in PubMed, 1 synthesis or guideline pooled it, 198 citations in OpenAlex.
- Understanding AMD by analogy: systematic review of lipid-related common pathogenic mechanisms in AMD, AD, AS and GN.Lipids in health and disease · 2018Pooled it
- Pathology after eculizumab in dense deposit disease and C3 GN.Journal of the American Society of Nephrology : JASN · 2012Trial
- Complement Profiling in Glomerular Disease: Insights from Laser Microdissection and Mass Spectrometry.Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- Thrombosis in paroxysmal nocturnal hemoglobinuria in the complement inhibitor era: mechanisms, risk stratification, and clinical management.International journal of hematology · 2026Review
- Update in the diagnosis of complement-mediated thrombotic microangiopathy/atypical hemolytic uremic syndrome.Hematology. American Society of Hematology. Education Program · 2025Review
- Article
- Revisiting Glomerulopathy in Clusterin Knockout Mice: A Mouse Model of Human Immunotactoid Glomerulopathy.Nephrology (Carlton, Vic.) · 2025Article
- Complement System Inhibitors in Nephrology: An Update-Narrative Review.International journal of molecular sciences · 2025Review
- The Role of von Willebrand Factor in the Pathogenesis of C3 Glomerulopathy.Kidney international reports · 2025Article
- Proteomic Insights into IgA Nephropathy: A Comprehensive Analysis of Differentially Expressed Proteins in the Kidney.ACS omega · 2025Article
- Expert Discussion on Immune Complex-Mediated Membranoproliferative Glomerulonephritis: Challenges and Considerations.Advances in therapy · 2025Article
- Age-related TFEB downregulation in proximal tubules causes systemic metabolic disorders and occasional apolipoprotein A4-related amyloidosis.JCI insight · 2024Article
- Review
- Plasma proteomics of acute tubular injury.Nature communications · 2024Article
- Complement and platelets: prothrombotic cell activation requires membrane attack complex-induced release of danger signals.Blood advances · 2023Article
- Complement: Functions, location and implications.Immunology · 2023Review
- Recurrent C3 Glomerulonephritis along with BK-Virus-Associated Nephropathy after Kidney Transplantation: A Case Report.Medicina (Kaunas, Lithuania) · 2023Article
- Proteomic Analysis of Complement Proteins in Glomerular Diseases.Kidney international reports · 2023Article
- Alternative pathway diagnostics.Immunological reviews · 2023Review
- C3 glomerulopathies: dense deposit disease and C3 glomerulonephritis.Frontiers in medicine · 2023Review
36 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Dense Deposit Disease (DDD), or membranoproliferative glomerulonephritis type II, is a rare renal disease characterized by dense deposits in the mesangium and along the glomerular basement membranes that can be seen by electron microscopy. Although these deposits contain complement factor C3, as determined by immunofluorescence microscopy, their precise composition remains unknown. To address this question, we used mass spectrometry to identify the proteins in laser microdissected glomeruli isolated from paraffin-embedded tissue of eight confirmed cases of DDD. Compared to glomeruli from five control patients, we found that all of the glomeruli from patients with DDD contain components of the alternative pathway and terminal complement complex. Factor C9 was uniformly present as well as the two fluid-phase regulators of terminal complement complex clusterin and vitronectin. In contrast, in nine patients with immune complex-mediated membranoproliferative glomerulonephritis, glomerular samples contained mainly immunoglobulins and complement factors C3 and C4. Our study shows that in addition to fluid-phase dysregulation of the alternative pathway, soluble components of the terminal complement complex contribute to glomerular lesions found in DDD.
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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.