ReviewClinical & developmental immunology2012
Kidney diseases caused by complement dysregulation: acquired, inherited, and still more to come.
Review in Clinical & developmental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- C3 glomerulopathy associated with both hypertensive retinopathy and purtscher-like retinopathy.American journal of ophthalmology case reports · 2022Article
- Predicting COVID-19-Comorbidity Pathway Crosstalk-Based Targets and Drugs: Towards Personalized COVID-19 Management.Biomedicines · 2021Article
- Sustained activation of C3aR in a human podocyte line impairs the morphological maturation of the cells.Molecular medicine reports · 2020Article
- Diverse Clinical Presentations of C3 Dominant Glomerulonephritis.Frontiers in medicine · 2020Article
- NLRP3 is Required for Complement-Mediated Caspase-1 and IL-1beta Activation in ICH.Journal of molecular neuroscience : MN · 2017Article
- Thrombotic microangiopathy associated with synthetic cannabinoid receptor agonists.Stem cell investigation · 2017Article
- Complement involvement in kidney diseases: From physiopathology to therapeutical targeting.World journal of nephrology · 2015Review
- American Society of Nephrology clinical pathological conference.Clinical journal of the American Society of Nephrology : CJASN · 2014Article
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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
Inherited and acquired dysregulation of the complement alternative pathway plays an important role in multiple renal diseases. In recent years, the identification of disease-causing mutations and genetic variants in complement regulatory proteins has contributed significantly to our knowledge of the pathogenesis of complement associated glomerulopathies. In these diseases defective complement control leading to the deposition of activated complement products plays a key role. Consequently, complement-related glomerulopathies characterized by glomerular complement component 3 (C3) deposition in the absence of local immunoglobulin deposits are now collectively described by the term "C3 glomerulopathies." Therapeutic strategies for reestablishing complement regulation by either complement blockade with the anti-C5 monoclonal antibody eculizumab or plasma substitution have been successful in several cases of C3 glomerulopathies. However, further elucidation of the underlying defects in the alternative complement pathway is awaited to develop pathogenesis-specific therapies.
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