ReviewMolecular immunology2011
Dense deposit disease.
Review in Molecular immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 96 citations in OpenAlex.
- Article
- Review
- Favorable outcome in children with dense deposit disease with the use of long-term mycophenolate mofetil and high-dose alternate-day steroids.Pediatric nephrology (Berlin, Germany) · 2025Article
- Clinical Remission and Reduction of Circulating Nephritic Factors by Combining Rituximab With Belimumab in a Case of Complement Factor 3 Glomerulopathy.Kidney international reports · 2024Article
- Hilar lymphadenopathy, development of tubulointerstitial nephritis, and dense deposit disease following Pfizer-BioNTech COVID-19 vaccination.CEN case reports · 2023Article
- Clinico-Pathogenic Similarities and Differences between Infection-Related Glomerulonephritis and C3 Glomerulopathy.International journal of molecular sciences · 2023Review
- C3 glomerulopathies: dense deposit disease and C3 glomerulonephritis.Frontiers in medicine · 2023Review
- C3 glomerulopathy: Understanding an ultra-rare complement-mediated renal disease.American journal of medical genetics. Part C, Seminars in medical genetics · 2022Review
- Outcome of C3 glomerulopathy patients: largest single-centre experience from South Asia.Journal of nephrology · 2020Article
- Nephritic Factors: An Overview of Classification, Diagnostic Tools and Clinical Associations.Frontiers in immunology · 2019Review
- Complement-mediated renal diseases after kidney transplantation - current diagnostic and therapeutic options inWorld journal of transplantation · 2018Review
- Timing and mechanism of conceptus demise in a complement regulatory membrane protein deficient mouse.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018Article
- Prevention of Fatal C3 Glomerulopathy by Recombinant Complement Receptor of the Ig Superfamily.Journal of the American Society of Nephrology : JASN · 2018Article
- Retinal Basal Laminar Deposits in Complement fH/fP Mouse Model of Dense Deposit Disease.Investigative ophthalmology & visual science · 2018Article
- Treating C3 glomerulopathy with eculizumab.BMC nephrology · 2018Article
- Disease-linked mutations in factor H reveal pivotal role of cofactor activity in self-surface-selective regulation of complement activation.The Journal of biological chemistry · 2017Article
- C5 inhibition prevents renal failure in a mouse model of lethal C3 glomerulopathy.Kidney international · 2017Article
- Complement in Non-Antibody-Mediated Kidney Diseases.Frontiers in medicine · 2017Review
- Complement related kidney diseases: Recurrence after transplantation.World journal of transplantation · 2016Review
- Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways.Kidney international reports · 2016Review
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 3 institutions in 2 countries.
Funding
Abstract
Dense deposit disease (DDD) is an orphan disease that primarily affects children and young adults without sexual predilection. Studies of its pathophysiology have shown conclusively that it is caused by fluid-phase dysregulation of the alternative pathway of complement, however the role played by genetics and autoantibodies like C3 nephritic factors must be more thoroughly defined if we are to make an impact in the clinical management of this disease. There are currently no mechanism-directed therapies to offer affected patients, half of whom progress to end stage renal failure disease within 10 years of diagnosis. Transplant recipients face the dim prospect of disease recurrence in their allografts, half of which ultimately fail. More detailed genetic and complement studies of DDD patients may make it possible to identify protective factors prognostic for naïve kidney and transplant survival, or conversely risk factors associated with progression to renal failure and allograft loss. The pathophysiology of DDD suggests that a number of different treatments warrant consideration. As advances are made in these areas, there will be a need to increase healthcare provider awareness of DDD by making resources available to clinicians to optimize care for DDD patients.
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.