ArticleKidney international reports2023
Proteomic Analysis of Complement Proteins in Glomerular Diseases.
Article in Kidney international reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The trial behind it
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- Complement and kidney diseases: unlocking the opportunity of targeted treatments for glomerular diseases, including IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2026Review
- Complement Inhibition in the Clinic: Are We Doing Enough to Protect Patients From Infection?European journal of immunology · 2026Review
- 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
- Renal Involvement in Pediatric Small-Vessel Vasculitis: A Comprehensive Review of Clinical Impact, Diagnosis, and Management.Medical sciences (Basel, Switzerland) · 2026Review
- Complement Profiling in Glomerular Disease: Insights from Laser Microdissection and Mass Spectrometry.Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- Proteomic Profiling of Complement Components in Glomerular Disease.Laboratory investigation; a journal of technical methods and pathology · 2026Article
- Update in the diagnosis of complement-mediated thrombotic microangiopathy/atypical hemolytic uremic syndrome.Hematology. American Society of Hematology. Education Program · 2025Review
- Rare and rapidly progressive crescentic proliferative glomerulonephritis with monoclonal immunoglobulin deposits: a case series study.Renal failure · 2025Article
- Transcriptomic Signatures in IgA Nephropathy: From Renal Tissue to Precision Risk Stratification.International journal of molecular sciences · 2025Review
- Spatial proteomics to discover aging-associated alterations in the renal tubulointerstitium.Clinical proteomics · 2025Article
- Expert Discussion on Immune Complex-Mediated Membranoproliferative Glomerulonephritis: Challenges and Considerations.Advances in therapy · 2025Article
- Clinical characteristics and short term outcomes of childhood immune complex membranoproliferative glomerulonephritis and C3 glomerulopathy: a single centre retrospective study.BMC nephrology · 2025Article
- Review
- Clinical significance of concomitant IgM and C3 deposition in patients with focal segmental glomerulosclerosis.Journal of nephrology · 2025Article
- Exploring the causal effect of complement and IgA nephropathy-a Mendelian randomization study.Renal failure · 2024Article
- Complement Activation in Nephrotic Glomerular Diseases.Biomedicines · 2024Review
- Urinary complement biomarkers in immune-mediated kidney diseases.Frontiers in immunology · 2024Review
- Novel biomarkers and pathophysiology of membranous nephropathy: PLA2R and beyond.Clinical kidney journal · 2024Review
- ANCA-Negative Pauci-Immune Glomerulonephritis: A Review.Glomerular diseasesReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Complement plays an important role in the pathogenesis of glomerulonephritis (GN). Even though the underlying etiology of GN might be different, complement activation with subsequent glomerular deposition of complement proteins result in glomerular injury and progression of the lesions. Routine immunofluorescence microscopy (IF) includes staining for only complement factors C3c and C1q. Therefore, with regard to evaluation of the complement pathways, routine kidney biopsy provides only limited information. Methods: In this study, using laser microdissection of glomeruli followed by mass spectrometry, complement proteins and pathways involved in GN were analyzed. Results: We found that C3 followed by C9 are the most abundant complement proteins in GN, indicating activation of classical or lectin or alternative, and terminal pathways, either exclusively or in a combination of pathways. Furthermore, depending on the type of GN, C4A and/or C4B were also present. Therefore, membranous nephropathy (MN), fibrillary GN, and infection-related GN showed C4A dominant pathways, whereas lupus nephritis (LN), proliferative GN with monoclonal Ig deposits, monoclonal Ig deposition disease (MIDD), and immunotactoid glomerulopathy showed C4B dominant pathways. Significant deposition of complement regulatory proteins, factor H-related protein-1 (FHR-1) and factor H-related protein-5 (FHR-5), were also detected in most GN. Conclusions: This study shows accumulation of specific complement proteins in GN. The complement pathways, complement proteins, and the amount of complement protein deposition are variable in different types of GN. Selective targeting of complement pathways may be a novel option in the treatment of GN.
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