ArticleWorld journal of nephrology2015
Update on immunoglobulin A nephropathy, Part I: Pathophysiology.
Article in World journal of nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Metabolomic profiling in IgA nephropathy: urinary and salivary biomarker insights.BMC nephrology · 2026Article
- Present and Future of IgA Nephropathy and Membranous Nephropathy Immune Monitoring: Insights from Molecular Studies.International journal of molecular sciences · 2023Review
- Rituximab use in adult glomerulopathies and its rationale.Jornal brasileiro de nefrologia · 2020Review
- Characterization of glomerular extracellular matrix in IgA nephropathy by proteomic analysis of laser-captured microdissected glomeruli.BMC nephrology · 2019Article
- Salivary microbial analysis of Chinese patients with immunoglobulin A nephropathy.Molecular medicine reports · 2019Article
- Decreased Expression of Urinary Mammalian Target of Rapamycin mRNA Is Related to Chronic Renal Fibrosis in IgAN.Disease markers · 2019Article
- IgA nephropathy: clearance kinetics of IgA-containing immune complexes.Seminars in immunopathology · 2018Review
- Why, when and how should immunosuppressive therapy considered in patients with immunoglobulin A nephropathy?Clinical and experimental immunology · 2016Review
- Update on immunoglobulin a nephropathy. Part II: Clinical, diagnostic and therapeutical aspects.World journal of nephrology · 2016Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin A (IgA) nephropathy is one of the most common glomerulonephritis and its frequency is probably underestimated because in most patients the disease has an indolent course and the kidney biopsy is essential for the diagnosis. In the last years its pathogenesis has been better identified even if still now several questions remain to be answered. The genetic wide association studies have allowed to identifying the relevance of genetics and several putative genes have been identified. The genetics has also allowed explaining why some ancestral groups are affected with higher frequency. To date is clear that IgA nephropathy is related to auto antibodies against immunoglobulin A1 (IgA1) with poor O-glycosylation. The role of mucosal infections is confirmed, but which are the pathogens involved and which is the role of Toll-like receptor polymorphism is less clear. Similarly to date whether the disease is due to the circulating immunocomplexes deposition on the mesangium or whether the antigen is already present on the mesangial cell as a "lanthanic" deposition remains to be clarified. Finally also the link between the mesangial and the podocyte injury and the tubulointerstitial scarring, as well as the mechanisms involved need to be better clarified.
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