ReviewSpringer seminars in immunopathology1982
Mesangial IgA nephritis.
Review in Springer seminars in immunopathology, 1982. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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Who cites it
8 citing papers in PubMed, 30 citations in OpenAlex.
- Uncoupling of glomerular IgA deposition and disease progression in alymphoplasia mice with IgA nephropathy.PloS one · 2014Article
- Immunopathogenesis of experimental IgA nephropathy.Springer seminars in immunopathology · 1994Review
- Response of circulating immune complexes to food challenge in relapsing IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 1987Article
- Clinical and therapeutic studies in mesangial immunoglobulin A glomerulonephritis.International urology and nephrology · 1987Article
- IgA-associated renal diseases: antibodies to environmental antigens in sera and deposition of immunoglobulins and antigens in glomeruli.Journal of clinical immunology · 1986Article
- Clearance of circulating IgA immune complexes is mediated by a specific receptor on Kupffer cells in mice.The Journal of experimental medicine · 1984Article
- Elution of antibodies to Mallory's hyaline from kidneys of patients with alcoholic liver disease and mesangial IgA deposits.Journal of clinical pathology · 1983Article
- The immunochemical characterization of mesangial IgA deposits.The American journal of pathology · 1983Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current data suggest that mesangial IgA nephritis is mediated by the mesangial deposition of soluble antigen-IgA class antibody complexes from the circulation. It is likely that common infectious gut flora and dietary antigens contribute to the immune complex load. Defects in antigen exclusion at the mucosa, in the control of IgA production, and in immune complex clearance are postulated to account for each of the recognized clinical syndromes. As yet no effective treatment is available, and a detailed analysis of the mediation pathways will be required before prevention or therapy can be attempted.
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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.