ArticleKidney international2020
Atypical hemolytic uremic syndrome associated with a factor B genetic variant and fluid-phase complement activation: an exception to the rule?
Article in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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
6 citing papers in PubMed, 8 citations in OpenAlex.
- Nephrogenomics, precision medicine and the role of genetic testing in adult kidney disease management.Nature reviews. Nephrology · 2025Review
- Molecular mimicry, hyperactive immune system, and SARS-COV-2 are three prerequisites of the autoimmune disease triangle following COVID-19 infection.International immunopharmacology · 2022Review
- Functional variant rs12614 inFrontiers in immunology · 2022Article
- Vitamin D deficiency: concern for rheumatoid arthritis and COVID-19?Molecular and cellular biochemistry · 2021Review
- Factor D Inhibition Blocks Complement Activation Induced by Mutant Factor B Associated With Atypical Hemolytic Uremic Syndrome and Membranoproliferative Glomerulonephritis.Frontiers in immunology · 2021Article
- Combination of a Novel Genetic Variant inFrontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gain-of-function variants in CFB encoding factor B (FB), a component of the alternative pathway C3 convertase, have been reported in a minority of patients with aHUS and result in massive C3 activation. Zhang et al. describe the functional characterization of a novel FB variant (p.Ser367Arg) that they identified in 2 unrelated aHUS pedigrees who had undetectable C3 levels. The mutant FB caused strong C3 cleavage in fluid-phase but also C3 deposition on cell surface. This commentary addresses the implications of these findings for understanding the complexity of complement-related genetic renal diseases.
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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.