ReviewNature reviews. Nephrology2016
Anti-complement-factor H-associated glomerulopathies.
Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses 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
59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 107 citations in OpenAlex.
- Guidelines on the Use of Therapeutic Apheresis in Clinical Practice-Evidence-Based Approach From the Writing Committee of the American Society for Apheresis: The Tenth Special Issue.Journal of clinical apheresis · 2026Guideline
- Variants in complement genes are uncommon in patients with anti-factor H autoantibody-associated atypical hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2023Pooled it
- Immunoglobulin Isotype Profiling of Anti-Factor H Autoantibodies in Complement-Mediated Diseases.International journal of laboratory hematology · 2026Article
- IPNA clinical practice recommendations for the management of aHUS and secondary TMA in children.Pediatric nephrology (Berlin, Germany) · 2026Article
- 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
- Obinutuzumab in kidney transplantation: Past, present, and future.World journal of transplantation · 2025Review
- Comprehensive genetic analysis and genotype-phenotype correlations in pediatric patients with atypical hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2025Article
- Discovery and characterization of vertebrate sialoglycan-binding proteins.Seminars in immunology · 2025Review
- C3 Glomerulonephritis Associated With Unusual IgG4 Antifactor H in IgG4-related Disease.Kidney medicine · 2025Article
- The complement system in autoimmune diseases: pathogenesis, diagnostic markers, and therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Atypical Hemolytic Uremic Syndrome: A Review of Complement Dysregulation, Genetic Susceptibility and Multiorgan Involvement.Journal of clinical medicine · 2025Review
- Article
- Protein-losing enteropathy as a new phenotype in atypical hemolytic uremic syndrome caused by CD46 gene mutation.Pediatric nephrology (Berlin, Germany) · 2024Review
- Managing anti-factor H antibody-associated hemolytic uremic syndrome: time for consensus.Pediatric nephrology (Berlin, Germany) · 2024Article
- Complement factor H in molecular regulation of angiogenesis.Medical review (2021) · 2024Review
- Abbreviated protocol of plasma exchanges for patients with anti-factor H associated hemolytic uremic syndrome.Pediatric nephrology (Berlin, Germany) · 2024Article
- An unusual case of adult-onset still's disease complicated with anti-complement factor H antibodies associated atypical haemolytic uraemic syndrome.BMC nephrology · 2024Article
- Factor H-related protein 1 in systemic lupus erythematosus.Frontiers in immunology · 2024Article
- Novel immunochromatographic test for rapid detection of anti-factor H autoantibodies with an assessment of its clinical relevance.Frontiers in immunology · 2024Article
- The human factor H protein family - an update.Frontiers in immunology · 2024Review
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atypical haemolytic uraemic syndrome (aHUS), an important cause of acute kidney injury, is characterized by dysregulation of the complement pathway, frequent need for dialysis, and progression to end-stage renal disease. Autoantibodies against complement factor H (FH), the main plasma regulatory protein of the alternative pathway of the complement system, account for a considerable proportion of children with aHUS. The autoantibodies are usually associated with the occurrence of a homozygous deletion in the genes encoding the FH-related proteins FHR1 and FHR3. High levels of autoantibodies, noted at the onset of disease and during relapses, induce functional deficiency of FH, whereas their decline, in response to plasma exchanges and/or immunosuppressive therapy, is associated with disease remission. Management with plasma exchange and immunosuppression is remarkably effective in inducing and maintaining remission in aHUS associated with FH autoantibodies, whereas terminal complement blockade with eculizumab is considered the most effective therapy in other forms of aHUS. Anti-FH autoantibodies are also detected in a small proportion of patients with C3 glomerulopathies, which are characterized by chronic glomerular injury mediated by activation of the alternative complement pathway and predominant C3 deposits on renal histology.
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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.