ReviewClinical kidney journal2025
Recent advances in pathogenetic concepts and disease modeling of IgA nephropathy.
Review in Clinical kidney journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- IgA Nephropathy: Mechanisms, Risk Stratification, and Precision Therapy.Diagnostics (Basel, Switzerland) · 2026Review
- Gut-kidney axis in IgA nephropathy: mechanisms linking microbiota dysbiosis to immune dysregulation, Gd-IgA1 generation, and renal injury.Frontiers in immunology · 2026Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IgA nephropathy (IgAN) is the most common form of glomerulonephritis and affected patients are at high risk of developing kidney failure over time. Recent molecular studies have led to substantial new insights into the pathogenesis of IgAN. This involves the identification of genetic risk factors in genome-wide association studies, the use of multi-omics approaches to integrate big data, the recognition of the importance of the gut-kidney axis, the role of plasma cells in the production of IgA and IgG, the potential specificity of circulating IgA for mesangial antigens, and the activation of the complement system with subsequent damage to glomerular cells. These fundamental insights were governed by the use of various animal models involving mesangial deposition of IgA, inflammation and glomerular injury. This review summarizes recently identified pathophysiological mechanisms as well as animal models of IgAN and provides an updated view on the molecular events that underlie IgAN.
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Registered trials
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