ReviewFrontiers in medicine2023
C3 glomerulopathies: dense deposit disease and C3 glomerulonephritis.
Review in Frontiers in medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Time to move to a cluster-based management of C3G/IC-MPGN.Pediatric nephrology (Berlin, Germany) · 2026Article
- Novel treatment strategies for C3 glomerulopathy: complement blockade.International urology and nephrology · 2026Review
- C3 glomerulopathy in transplant "like yet unlike native": Pathophysiology, recent advances in therapeutics and evolving paradigms.World journal of transplantation · 2026Review
- Diagnosis and treatment in adult patients with C3 glomerulopathy in Japan: a real-world survey.Clinical and experimental nephrology · 2026Article
- A very rare cause of oliguric acute kidney disease: crescentic C3 glomerulopathy.Oxford medical case reports · 2025Article
- Review
- Article
- Clinical characteristics and short term outcomes of childhood immune complex membranoproliferative glomerulonephritis and C3 glomerulopathy: a single centre retrospective study.BMC nephrology · 2025Article
- Acquired drivers of C3 glomerulopathy.Clinical kidney journal · 2025Review
- Iptacopan treatment for recurrent dense deposit disease after kidney transplant: A case report.SAGE open medical case reports · 2025Article
- Effective long-term treatment with moss-produced factor H by overcoming the antibody response in a mouse model of C3G.Frontiers in immunology · 2025Article
- Challenges in the Diagnosis and Management of Immune Complex-Mediated Membranoproliferative Glomerulonephritis and Complement 3 Glomerulopathy.Kidney international reports · 2025Review
- Updates on C3 Glomerulopathy in Kidney Transplantation: Pathogenesis and Treatment Options.International journal of molecular sciences · 2024Review
- Plasma and Kidney Proteome Profiling Combined with Laser Capture Microdissection Reveal Large Increases in Immunoglobulins with Age.Proteomes · 2024Article
- Morphological Changes in the Saw-Tooth Pattern of Cuticular Drusen Associated with Immune Complex-Mediated Membranous Proliferative Glomerulonephritis Type III: A Case Report.Case reports in ophthalmologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) are types of membranoproliferative glomerulonephritis classified as C3 glomerulopathies. These conditions are characterized by an increased number of intraglomerular cells and diffuse thickening of the glomerular capillary walls, along with the deposition of C3 and minimal or absent immunoglobulin deposits. The underlying cause of both DDD and C3Gn is an abnormal activation of the alternative complement pathway, which can result from acquired or genetic alteration. In acquired forms of DDD and C3GN, the dysregulation of the alternative pathway is commonly induced by the presence of C3 nephritic factors (C3NeFs), which are autoantibodies that stabilize C3 convertase. Both DDD and C3GN can affect individuals of any age, but DDD is primarily diagnosed in children, whereas C3GN tends to be diagnosed at a significantly higher age. The presenting features of these diseases are variable and may include proteinuria, hematuria, hypertension, or kidney failure. A common finding in these diseases is low serum C3 levels with normal serum C4 levels. Chronic deterioration of renal function is commonly observed in DDD and C3GN, often leading to end-stage renal disease (ESRD), especially in DDD. Kidney transplantation outcomes in patients with these conditions are characterized by histological recurrence, which may contribute to higher rates of allograft failure.
Indexed as
Identifiers
What OpenQuestion holds
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.