ReviewClinical and experimental nephrology2017
C3 glomerulopathy and current dilemmas.
Review in Clinical and experimental nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Pharmacokinetics, Pharmacodynamics, Safety, and Tolerability of HSK39297 in Chinese Healthy Subjects: A Phase 1 Clinical Trial.Clinical and translational science · 2025Trial
- Poststreptococcal Glomerulonephritis Secondary to Bacterial Vaginosis, Complicated by Hemolytic Anemia and Thrombocytopenia.Internal medicine (Tokyo, Japan) · 2026Article
- Review
- Evaluation of the significance of complement-related genes mutations in atypical postinfectious glomerulonephritis: a pilot study.International urology and nephrology · 2024Article
- Article
- Clinical and pathological features of 52 patients with glomerulonephritis with dominant C3.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Clinico-Pathogenic Similarities and Differences between Infection-Related Glomerulonephritis and C3 Glomerulopathy.International journal of molecular sciences · 2023Review
- Article
- 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
- A case of C3 glomerulopathy with nephritis-associated plasmin receptor positivity without a history of streptococcal infection.CEN case reports · 2022Article
- Genetic analysis of CFH and MCP in Egyptian patients with immune-complex proliferative glomerulonephritis.Frontiers in immunology · 2022Article
- Utility of immunohistochemistry with C3d in C3 glomerulopathy.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Clinicopathological features of C3 glomerulopathy in children: a single-center experience.Pediatric nephrology (Berlin, Germany) · 2020Article
- Clinical and Pathophysiological Insights Into Immunological Mediated Glomerular Diseases in Childhood.Frontiers in pediatrics · 2020Review
- Complement and Complement Targeting Therapies in Glomerular Diseases.International journal of molecular sciences · 2019Review
- Characteristics of membranoproliferative glomerulonephritis based on a new classification at a single center.Clinical and experimental nephrology · 2019Article
- Complement your knowledge with a rare cause of pauci-immune glomerulonephritis.Clinical rheumatology · 2018Article
- The role of the alternative pathway of complement activation in glomerular diseases.Clinical and experimental medicine · 2018Review
- Clinical features and pathogenesis of membranoproliferative glomerulonephritis: a nationwide analysis of the Japan renal biopsy registry from 2007 to 2015.Clinical and experimental nephrology · 2018Article
- The PD-1/PD-L1 Inhibitory Pathway is Altered in Primary Glomerulonephritides.Archivum immunologiae et therapiae experimentalis · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C3 glomerulopathy (C3G) is a recently identified disease entity caused by dysregulation of the alternative complement pathway, and dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) are its components. Because laboratory detection of complement dysregulation is still uncommon in practice, "dominant C3 deposition by two orders greater than that of immunoglobulins in the glomeruli by immunofluorescence", as stated in the consensus report, defines C3G. However, this morphological definition possibly includes the cases with glomerular diseases of different mechanisms such as post-infectious glomerulonephritis. In addition, the differential diagnosis between DDD and C3GN is often difficult because the distinction between these two diseases is based solely on electron microscopic features. Recent molecular and genetic advances provide information to characterize C3G. Some C3G cases are found with genetic abnormalities in complement regulatory factors, but majority of cases seem to be associated with acquired factors that dysregulate the alternative complement pathway. Because clinical courses and prognoses among glomerular diseases with dominant C3 deposition differ, further understanding the background mechanism, particularly complement dysregulation in C3G, is needed. This may resolve current dilemmas in practice and shed light on novel targeted therapies to remedy the dysregulated alternative complement pathway in C3G.
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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.