ReviewJournal of clinical medicine2022
New Treatment Strategies for IgA Nephropathy: Targeting Plasma Cells as the Main Source of Pathogenic Antibodies.
Review in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Refractory IgA Nephropathy: A Challenge for Future Nephrologists.Medicina (Kaunas, Lithuania) · 2024Pooled it
- Preservation of Humoral Immunity and Response to Vaccination in Patients With IgAN Treated With Felzartamab.Kidney international reports · 2026Article
- IgA nephropathy management: what does the future hold?Kidney international supplements · 2026Review
- Structure and function of therapeutic antibodies approved by the US FDA in 2025.Antibody therapeutics · 2026Review
- Comprehensive Analysis of IgA Nephropathy Causal Factors in Plasma Proteins, Immune Cell Types, and Immune Cell Traits.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- Single-dose rituximab as induction therapy in adult IgA vasculitis with rapidly progressive glomerulonephritis: a case report with peripheral blood CD19⁺ B-cell monitoring.CEN case reports · 2026Article
- A rabbit anti-human CD38 antibody for eliminating daratumumab and isatuximab interference in immunohematology testing.Frontiers in immunology · 2026Article
- Review
- Prospective Pilot Study of Plasma Cell-Targeted Therapy With Bortezomib in Refractory IgA Nephropathy.Kidney international reports · 2025Article
- Pharmacological interventions in IgA nephropathy: protocol for a living systematic review and network meta-analysis.BMJ open · 2025Article
- Treating IgA Nephropathy: Looking at the Future Without Forgetting the Past.Journal of clinical medicine · 2025Review
- Recent advances in pathogenetic concepts and disease modeling of IgA nephropathy.Clinical kidney journal · 2025Review
- Comparing adolescent glomerular disease clinical outcomes to the clinical outcomes in childhood, young adult, and adult-onset glomerular disease in the CureGN database.Pediatric nephrology (Berlin, Germany) · 2025Article
- To establish and validate autophagy related biomarkers for the diagnosis of IgA nephropathy.Scientific reports · 2025Article
- Mechanistic insights into Shenqi Dihuang decoction in the treatment of immunoglobulin a nephropathy.Frontiers in pharmacology · 2025Article
- Exploring Novel Adverse Events of Nefecon.Kidney international reports · 2024Article
- Effect of Telitacicept on Circulating Gd-IgA1 and IgA-Containing Immune Complexes in IgA Nephropathy.Kidney international reports · 2024Article
- An Update on Current Therapeutic Options in IgA Nephropathy.Journal of clinical medicine · 2024Review
- Efficacy and safety of biologic agents for IgA nephropathy: A protocol for systematic review and meta-analysis.PloS one · 2024Article
- Causal association between peripheral immune cells and IgA nephropathy: a Mendelian randomization study.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin A nephropathy (IgAN) is a rare autoimmune disorder and the leading cause of biopsy-reported glomerulonephritis (GN) worldwide. Disease progression is driven by the formation and deposition of immune complexes composed of galactose-deficient IgA1 (Gd-IgA1) and Gd-IgA1 autoantibodies (anti-Gd-IgA1 antibodies) in the glomeruli, where they trigger complement-mediated inflammation that can result in loss of kidney function and end-stage kidney disease (ESKD). With the risk of progression and limited treatment options, there is an unmet need for therapies that address the formation of pathogenic Gd-IgA1 antibody and anti-Gd-IgA1 antibody-containing immune complexes. New therapeutic approaches target immunological aspects of IgAN, including complement-mediated inflammation and pathogenic antibody production by inhibiting activation or promoting depletion of B cells and CD38-positive plasma cells. This article will review therapies, both approved and in development, that support the depletion of Gd-IgA1-producing cells in IgAN and have the potential to modify the course of this disease. Ultimately, we propose here a novel therapeutic approach by depleting CD38-positive plasma cells, as the source of the autoimmunity, to treat patients with IgAN.
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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.