ReviewClinical kidney journal2023
Targeting complement in IgA nephropathy.
Review in Clinical kidney journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.
- Efficacy and safety of complement inhibitors in IgAN: a systematic review and meta-analysis.International urology and nephrology · 2026Pooled it
- Efficacy and safety of BAFF/APRIL dual antagonists in IgA nephropathy: a systematic review and meta-analysis of randomized controlled trials.BMC nephrology · 2025Pooled it
- Pharmacokinetics, Pharmacodynamics, Safety, and Tolerability of HSK39297 in Chinese Healthy Subjects: A Phase 1 Clinical Trial.Clinical and translational science · 2025Trial
- Proteinuria in adolescence.Pediatric nephrology (Berlin, Germany) · 2026Review
- Eculizumab for rapidly progressive glomerulonephritis in children.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026Article
- Per- and polyfluoroalkyl substances and kidney disease: Genetic associations and computational prioritization of candidate toxicogenomic pathways.PLoS computational biology · 2026Article
- Update on IgA nephropathy: implications for treatment in IgA vasculitis: a guide for rheumatologists.Current opinion in rheumatology · 2026Review
- IgA nephropathy: an overview of the disease, its pathophysiology, and involvement of the gut-kidney axis.Kidney international supplements · 2026Review
- The Alternative Complement Pathway in IgA Nephropathy: A Podcast for Advanced Practice Providers.Advances in therapy · 2026Article
- Progress in immunological research on innate effectors in xenotransplantation.Surgery today · 2026Review
- Multi-omics triangulation identifies complement factor H as a genetically supported protective factor in IgA nephropathy.Clinical kidney journal · 2026Article
- Review
- Principles for Optimal Drug Selection in IgA Nephropathy-Time for Integrating Pathogenesis and Clinical Markers to Guide Therapy.Nephrology (Carlton, Vic.) · 2026Review
- New Anticomplement Drugs in Nephrology: Mechanism and Indication.Kidney & blood pressure research · 2026Review
- Mechanistic Insights and Therapeutic Advances of Anti-Inflammatory Biologics in Immune-Mediated Glomerulonephritis: A Narrative Review.Journal of inflammation research · 2026Review
- Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.Frontiers in medicine · 2026Review
- Short interference RNAs in glomerulonephritis: A mini review.BioImpacts : BI · 2026Review
- Aberrant signaling in tonsillar B cells producing pathogenicFrontiers in immunology · 2026Review
- Research progress on the lectin pathway of complement in IgA nephropathy.Frontiers in immunology · 2026Review
- Complement biomarkers in IgA nephropathy: current insights and clinical relevance.Frontiers in nephrology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Recent years have witnessed significant improvements in the understanding of the pathogenesis of IgAN and particularly, the pathogenic role of complement activation. The alternative complement pathway is the major complement cascade activator in IgAN, and glomerular C3 deposition has been shown to correlate with disease progression. In addition, several studies have provided insight into the pathogenic role of factor H-related proteins -1 and -5 in IgAN, as independent players in complement dysregulation. The lectin pathway has also been shown to be associated with the severity of IgAN. Glomerular deposition of C4d has been associated with increased histologic disease activity, faster decline in estimated glomerular filtration rate and higher risk of kidney failure. On the other hand, although overlooked in the Oxford classification, numerous studies have shown that the coexistence of thrombotic microangiopathy in IgAN is a significant indicator of a poorer prognosis. All the breakthroughs in the understanding of the contributing role of complement in IgAN have paved the way for the development of new complement-targeted therapies in this disease. Several ongoing trials are evaluating the efficacy of new agents against factor B (iptacopan, Ionis-FB-L
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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.