ArticleKidney international reports2022
Comparison of Complement Pathway Activation in Autoimmune Glomerulonephritis.
Article in Kidney international reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- Immune Deposits, Complement Activation, and <italic>APOL1</italic> Risk Variants in Focal Segmental Glomerulosclerosis.American journal of nephrology · 2026Article
- Complement diagnostics and therapeutics for the pediatric population: early successes and opportunities for further advancement.Frontiers in pharmacology · 2026Review
- Multi-omics analyses demonstrate complement dysregulation is involved in focal segmental glomerulosclerosis.Frontiers in immunology · 2026Article
- Emerging role of complement system in the induction of neuroinflammation in adenylosuccinate lyase deficiency disorder.Brain, behavior, & immunity - health · 2025Review
- Urinary Complement proteome strongly linked to diabetic kidney disease progression.Nature communications · 2025Article
- Proteomic Insights into IgA Nephropathy: A Comprehensive Analysis of Differentially Expressed Proteins in the Kidney.ACS omega · 2025Article
- Clinical Significance of Immune Deposits and Complement System Activation in FSGS: Findings from the Cure Glomerulonephropathy Network Study.Kidney360 · 2025Article
- Complement System and Adhesion Molecule Skirmishes in Fabry Disease: Insights into Pathogenesis and Disease Mechanisms.International journal of molecular sciences · 2024Review
- Unraveling the Role of Complement in Focal Segmental Glomerulosclerosis Pathogenesis: Insights and Challenges.Kidney international reports · 2024Article
- A Prospective Study on Complement Activation Distinguishes Focal Segmental Glomerulosclerosis from Minimal Change Disease.Kidney international reports · 2024Article
- Targeting complement in IgA nephropathy.Clinical kidney journal · 2023Review
- Urine and Plasma Complement Ba Levels During Disease Flares in Patients With Antineutrophil Cytoplasmic Autoantibody-Associated Vasculitis.Kidney international reports · 2023Article
- Recent Advances of Proteomics in Management of Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2023Review
- Glomerulonephritis: immunopathogenesis and immunotherapy.Nature reviews. Immunology · 2023Review
- CD44 Expression in Renal Tissue Is Associated with an Increase in Urinary Levels of Complement Components in Chronic Glomerulopathies.International journal of molecular sciences · 2023Article
- Causal effects of human serum metabolites on occurrence and progress indicators of chronic kidney disease: a two-sample Mendelian randomization study.Frontiers in nutrition · 2023Article
- Current understanding of the molecular mechanisms of circulating permeability factor in focal segmental glomerulosclerosis.Frontiers in immunology · 2023Review
- Can Urinary Complement Proteins Stratify Patients to Therapeutic Complement Inhibitors?Kidney international reports · 2022Article
- The role of the complement system in primary membranous nephropathy: A narrative review in the era of new therapeutic targets.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Studies on complement activation have implicated a combination of the classical pathway (CP), lectin pathway (LP), and alternative pathway (AP) in triggering the terminal pathway (TP) for each common autoimmune glomerulonephritis (GN). Evaluating different pathways simultaneously may help identify whether one is preferentially activated and, consequently, which is best to target for each disease. Methods: We followed 112 patients with focal segmental glomerular sclerosis (FSGS), membranous nephropathy (MN), IgA nephropathy (IgAN), lupus nephritis (LN), and antineutrophil cytoplasmic autoantibody-associated vasculitis (AAV) for a median duration of 22 (12-52) months. At the time of greatest clinical activity, we simultaneously evaluated urinary C3a (C3 convertase activity), C5a and sC5b-9 (TP), MASP-1 and MASP-2 (LP), C1q (CP), C4a (CP/LP), and Ba and Bb (AP). We evaluated the relation between activation fragments of the AP and CP/LP with the TP. Results: Urinary complement biomarkers for each pathway were associated with the severity of proteinuria. Fragments of the TP were higher among patients with FSGS and MN compared with patients with IgAN, LN, and AAV. For the AP, urinary Ba level was lower in those with IgAN and LN compared with those with FSGS. For the CP/LP, urinary C4a, MASP-1, and MASP-2 levels were similar between diseases whereas urinary C1q levels were lower in those with LN. For each GN, independent associations existed between the activation markers of the AP and CP/LP with the degree of TP activation, except for the AP in AAV, although perhaps underpowered. Conclusion: The AP and CP/LP contribute individually to the TP activation in autoimmune GN, and both seem to be valid potential therapeutic targets.
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Registered trials
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