ArticleKidney international2017
Circulating complement factor H-related proteins 1 and 5 correlate with disease activity in IgA nephropathy.
Article in Kidney international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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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.
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Who cites it
82 citing papers in PubMed, 141 citations in OpenAlex.
- From therapeutic lag to clinical trials: the changing landscape of pediatric IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2026Article
- Complement and kidney diseases: unlocking the opportunity of targeted treatments for glomerular diseases, including IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2026Review
- Advances in Complement Research: from Pathophysiology to Precision Medicine.Physiology (Bethesda, Md.) · 2026Review
- Plasma Proteomics in IgA Nephropathy: From Circulating Biomarkers to Molecular Endotypes.Cells · 2026Review
- The Alternative Complement Pathway in IgA Nephropathy: A Podcast for Advanced Practice Providers.Advances in therapy · 2026Article
- Biomarkers in the Management of Complement-Mediated Kidney Diseases in the Era of Complement Therapeutics.Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- Association of Complement Genetics with Outcomes in IgA Nephropathy.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- IgA nephropathy new therapies: from data in adults to application in children.Pediatric nephrology (Berlin, Germany) · 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
- Complement-Mediated Kidney Diseases: Role of Alternative Pathway in Glomerular Inflammation.Kidney international reports · 2026Review
- Dual Role of Factor H-Related Protein 1 in IgA Nephropathy Kidney Injury.Kidney international reports · 2026Article
- Complement biomarkers in IgA nephropathy: current insights and clinical relevance.Frontiers in nephrology · 2026Review
- Breaking tolerance in the glomerulus: complement as a driver and therapeutic target in IgA nephropathy.Frontiers in medicine · 2026Review
- Research progress on the lectin pathway of complement in IgA nephropathy.Frontiers in immunology · 2026Review
- Complement proteins associated with circulatory and glomerular IgA-containing immune complexes in patients with IgA nephropathy.Scientific reports · 2025Article
- Review
- Evaluation of Serum Complement Components in Pediatric IgA Vasculitis: A Case-Control Study.Children (Basel, Switzerland) · 2025Article
- Developing serum proteomics based prediction models of disease progression in ADPKD.Nature communications · 2025Article
- Complement System Inhibitors in Nephrology: An Update-Narrative Review.International journal of molecular sciences · 2025Review
- Chronic kidney disease enhances alternative pathway activity: a new paradigm.The Journal of clinical investigation · 2025Review
22 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
IgA nephropathy (IgAN) is a common cause of chronic kidney disease and end-stage renal failure, especially in young people. Due to a wide range of clinical outcomes and difficulty in predicting response to immunosuppression, we need to understand why and identify which patients with IgAN will develop progressive renal impairment. A deletion polymorphism affecting the genes encoding the complement factor H-related protein (FHR)-1 and FHR-3 is robustly associated with protection against IgAN. Some FHR proteins, including FHR-1 and FHR-5, antagonize the ability of complement factor H (fH), the major negative regulator of the complement alternative pathway, to inhibit complement activation on surfaces, a process termed fH deregulation. From a large cohort of patients, we demonstrated that plasma FHR-1 and the FHR-1/fH ratio were elevated in IgAN and associated with progressive disease. Plasma FHR-1 negatively correlated with eGFR but remained elevated in patients with IgAN with normal eGFR. Serum FHR5 was slightly elevated in IgAN but did not correlate with eGFR. Neither FHR5 levels nor the FHR-5/fH ratio was associated with progressive disease. However, higher serum FHR-5 levels were associated with a lack of response to immunosuppression, the presence of endocapillary hypercellularity, and histology scores of disease severity (the Oxford Classification MEST score). Thus, FHR-1 and FHR-5 have a role in IgAN disease progression.
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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.