ReviewSeminars in immunopathology2021
IgA glycosylation and immune complex formation in IgAN.
Review in Seminars in immunopathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 75 citations in OpenAlex.
- Targeting the B-Cell Activating Factor and a Proliferation-Inducing Ligand Pathway in IgAN: From Disease Pathogenesis to Clinical Trial Evidence.Kidney international reports · 2026Review
- Time-Updated Hematuria and Kidney Disease Progression in IgAN.Kidney international reports · 2026Article
- IgA nephropathy: an overview of the disease, its pathophysiology, and involvement of the gut-kidney axis.Kidney international supplements · 2026Review
- Forsythiaside A Alleviates Kidney Injury and Intestinal Epithelium Dysfunction in IgA Nephropathy by Inhibiting TLR4/NF-κB Signaling.The Kaohsiung journal of medical sciences · 2026Article
- Sialic Acids in Kidney Disease: Immune Regulation, Complement Activation and Glomerular Injury.Antioxidants (Basel, Switzerland) · 2026Review
- Multiplex Detection of Immunoglobulins Uncovers Intrathecal IgA Elevation in Multiple Sclerosis.Cells · 2026Article
- Lipidomic profiling reveals medium-chain acylcarnitines alterations as metabolic signatures in IgA nephropathy.BMC nephrology · 2026Article
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
- Poly-IgA immune complex as a monitoring biomarker of response to telitacicept in IgA nephropathy.Frontiers in immunology · 2026Article
- The efficacy and safety of telitacicept and its combination with glucocorticoids in IgA nephropathy: a retrospective cohort study.Frontiers in pharmacology · 2026Article
- Gut microbiota in Henoch-Schönlein purpura: from pathogenesis to therapeutic strategies.Frontiers in immunology · 2026Review
- Autoimmunity in IgA nephropathy.Frontiers in immunology · 2026Review
- Cross-phenotype integration of eQTL-based Mendelian randomization and transcriptomics prioritizesFrontiers in immunology · 2026Article
- Targeted-release budesonide versus systemic corticosteroids in IgA nephropathy: a real-world comparative study.Frontiers in immunology · 2026Article
- Immune cells mediate the effect of plasma lipidomes on IgA nephropathy: a Mendelian randomization study.Renal failure · 2025Article
- Efficacy and safety of telitacicept in IgA nephropathy: a real-world study.Renal failure · 2025Article
- The importance of the degree of foot process effacement in evaluating the prognosis of IgA nephropathy.International urology and nephrology · 2025Article
- Review
- Predictive value of Gd-IgA1, poly-IgA in the treatment of IgA nephropathy with targeted-release formulation budesonide.Clinical kidney journal · 2025Article
- Glomerular galactose-deficient IgA1 and apoptosis inhibitor of macrophage staining in secondary IgA nephropathy associated with alcoholic cirrhosis.Journal of nephrology · 2025Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. This disease, discovered in 1968, is characterized by IgA-IgG glomerular immunodeposits with a mesangial pattern. It is thought that these immunodeposits originate from the immune complexes formed in the circulation. It is hypothesized that the pathogenesis of IgAN is driven by aberrant glycoforms of IgA1 (galactose-deficient IgA1, Gd-IgA1). Gd-IgA1, in genetically susceptible individuals, represents the initiating factor for the formation of circulating immune complexes due to its recognition by IgG autoantibodies and the subsequent formation of pathogenic IgA1-IgG immune complexes. Complement activation through alternative and/or lectin pathways is likely playing an important role in the pathogenic properties of these complexes and may further upregulate local inflammatory responses and glomerular injury.
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What OpenQuestion holds
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.