ReviewSeminars in nephrology2024
Emerging Biochemical and Immunologic Mechanisms in the Pathogenesis of IgA Nephropathy.
Review in Seminars in nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Correlation of foot process effacement with clinicopathological features and short-term prognosis in IgA nephropathy.Annals of medicine · 2026Article
- Development of IgA nephropathy following risankizumab therapy for psoriatic arthritis: a case report.CEN case reports · 2026Article
- Successful 6-year follow-up of treatment for IgA nephropathy complicated by IgA-λ monoclonal gammopathy with multi-system damage: a case report.Frontiers in immunology · 2026Article
- Development and validation of a routine urinalysis-based risk stratification model for IgA nephropathy in a multicenter real-world hospital population.Frontiers in nephrology · 2026Article
- Review
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Authors and funding
9 authors.
Funding
Abstract
IgA nephropathy is a mesangioproliferative glomerular disease with significant morbidity and mortality. Most patients with IgA nephropathy develop kidney failure in their lifetime, reducing their life expectancy by a decade. Since its first description in 1968, it has been established that kidneys of IgA nephropathy patients are injured as "innocent bystanders" by nephritogenic IgA1-containing immune complexes. Results from clinical, biochemical, immunologic, and genetic studies suggest a multistep pathogenetic mechanism. In genetically predisposed individuals, this process results in formation of circulating immune complexes due to the binding of IgG/IgA autoantibodies to the polymeric IgA1 molecules with incomplete O-glycosylation. This event is followed by the addition of other proteins, such as complement C3, resulting in the formation of nephritogenic immune complexes. These complexes are not effectively removed from the circulation, and some of them pass through the fenestration of glomerular endothelial cells to enter the mesangial space and activate mesangial cells. It is thought that the process is initiated by soluble immune complexes and that their accumulation results in the formation of immunodeposits that further amplify glomerular injury. Here we summarize current understanding of the pathogenesis of IgA nephropathy and discuss experimental model systems that can inform development of new therapeutic strategies and targets.
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