ReviewJournal of nephrology2018
Dominant C3 glomerulopathy: new roles for an old actor in renal pathology.
Review in Journal of nephrology, 2018. 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.
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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
6 citing papers in PubMed.
- Acute Kidney Injury in Monoclonal Gammopathies.Journal of clinical medicine · 2021Review
- Review
- Outcome of C3 glomerulopathy patients: largest single-centre experience from South Asia.Journal of nephrology · 2020Article
- Complement your knowledge with a rare cause of pauci-immune glomerulonephritis.Clinical rheumatology · 2018Article
- CFHR5 Nephropathy in a Greek-Cypriot Australian Family: Ancestry-Informed Precision Medicine.Kidney international reports · 2018Article
- Complement C3 Produced by Macrophages Promotes Renal Fibrosis via IL-17A Secretion.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, a number of reports have described dominant C3 deposits in renal biopsies of patients with infection-related glomerulonephritis (GN). While acute post-infectious GN and membranoproliferative GN are commonly characterized by immune deposits containing C3 and/or C4, the absence of immunoglobulin (Ig) and/or immune complexes at light or electron microscopy is a rather unusual observation. Dominant C3 deposition is believed to result from the alternative pathway of complement activation via the C3bBb "tickover" convertase. The actual occurrence of C3 glomerulopathy could be underestimated, since infection-related GN often quickly subsides without the need for a renal biopsy. A more thorough understanding of the pathways that lead to complement assembly and deposition within the kidney is needed to support a new classification of complement-related lesions, including entities such as dense deposit disease, (atypical) hemolytic-uremic syndrome, dominant C1q, CFHR5, C4d, and C3 glomerulopathies. We will briefly review recent work in this area, focusing on GN with selective complement C3 deposits.
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Registered trials
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