ArticleKidney international2010
Treatment with human complement factor H rapidly reverses renal complement deposition in factor H-deficient mice.
Article in Kidney international, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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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.
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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
59 citing papers in PubMed, 108 citations in OpenAlex.
- Truncated complement factor H Y402 gene therapy rescues C3 glomerulonephritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Moss-derived human complement factor H modulates retinal immune response and attenuates retinal degeneration.Journal of neuroinflammation · 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
- Developing Therapies for C3 Glomerulopathy: Report of the Kidney Health Initiative C3 Glomerulopathy Trial Endpoints Work Group.Clinical journal of the American Society of Nephrology : CJASN · 2024Article
- C3d-Targeted factor H inhibits tissue complement in disease models and reduces glomerular injury without affecting circulating complement.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Article
- Proof of concept of a new plasma complement Factor H from waste plasma fraction.Frontiers in immunology · 2024Article
- Moss-produced human complement factor H with modified glycans has an extended half-life and improved biological activity.Frontiers in immunology · 2024Article
- Anti-complement factor H (CFH) autoantibodies could delay pristane-induced lupus nephritis.Immunologic research · 2023Article
- Unleashing the power of complement activation: unraveling renal damage in human anti-glomerular basement membrane disease.Frontiers in immunology · 2023Review
- Physiology and pathology of the C3 amplification cycle: A retrospective.Immunological reviews · 2023Review
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
- The Rational Use of Complement Inhibitors in Kidney Diseases.Kidney international reports · 2022Review
- An Interdisciplinary Diagnostic Approach to Guide Therapy in C3 Glomerulopathy.Frontiers in immunology · 2022Article
- Amnion epithelial cells are an effective source of factor H and prevent kidney complement deposition in factor H-deficient mice.Stem cell research & therapy · 2021Article
- Gain-of-function factor H-related 5 protein impairs glomerular complement regulation resulting in kidney damage.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Complement activity is regulated in C3 glomerulopathy by IgG-factor H fusion proteins with and without properdin targeting domains.Kidney international · 2021Article
- Sugar Matters: Improving In Vivo Clearance Rate of Highly Glycosylated Recombinant Plasma Proteins for Therapeutic Use.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Murine Factor H Co-Produced in Yeast With Protein Disulfide Isomerase Ameliorated C3 Dysregulation in Factor H-Deficient Mice.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Total deficiency of complement factor H (CFH) is associated with dense deposit disease and atypical hemolytic uremic syndrome. CFH is the major regulator of the alternative pathway of complement activation and its complete deficiency results in uncontrolled C3 activation through this pathway and secondary C3 deficiency. Plasma infusion, as a source of CFH, has been used with variable success to treat renal disease associated with its deficiency. However, the risks of volume and protein overload limit this therapeutic approach. In this study, we investigated the efficacy of a purified human CFH (hCFH) preparation in Cfh-gene knockout mice. These mice spontaneously develop both secondary plasma C3 deficiency and a renal abnormality characterized by massive accumulation of C3 along the glomerular basement membrane. The renal lesion is analogous to human dense deposit disease. Treatment of knockout mice with hCFH resulted in rapid normalization of plasma C3 levels and resolution of the glomerular basement membrane C3 deposition. Long-term treatment of mice with hCFH was not possible because of the development of an immune response against hCFH. Hence, we suggest that hCFH can be an effective alternative therapy to plasma infusions in patients with renal disease associated with CFH deficiency.
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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.