ArticlePediatric nephrology (Berlin, Germany)2015
A case of C3 glomerulonephritis successfully treated with eculizumab.
Article in Pediatric nephrology (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 33 citations in OpenAlex.
- Long-term eculizumab treatment failure in C3 glomerulonephritis: two case reports.Clinical kidney journal · 2026Article
- Delayed Therapeutic Response to Oral Corticosteroids and Rituximab Leading to Dialysis Independence in a Patient with Treatment-resistant C3 Glomerulonephritis.Internal medicine (Tokyo, Japan) · 2026Article
- Contemporary Monoclonal Antibody Utilization in Glomerular Diseases.Mayo Clinic proceedings. Innovations, quality & outcomes · 2023Review
- Renal diseases and the role of complement: Linking complement to immune effector pathways and therapeutics.Advances in immunology · 2021Review
- Deposition of the Membrane Attack Complex in Healthy and Diseased Human Kidneys.Frontiers in immunology · 2020Review
- Eculizumab for pediatric dense deposit disease: A case report and literature review.Clinical nephrology. Case studies · 2020Article
- Nephritic Factors: An Overview of Classification, Diagnostic Tools and Clinical Associations.Frontiers in immunology · 2019Review
- Long-term Eculizumab Therapy in a Child With Refractory Immune Complex-Mediated Membranoproliferative Glomerulonephritis.Kidney international reports · 2018Article
- Treating C3 glomerulopathy with eculizumab.BMC nephrology · 2018Article
- Review
- Complement C5-inhibiting therapy for the thrombotic microangiopathies: accumulating evidence, but not a panacea.Clinical kidney journal · 2017Article
- Rituximab for Treatment of Membranoproliferative Glomerulonephritis and C3 Glomerulopathies.BioMed research international · 2017Review
- Severe active C3 glomerulonephritis triggered by immune complexes and inactivated after eculizumab therapy.Diagnostic pathology · 2016Article
- Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways.Kidney international reports · 2016Review
- Anti-complement-factor H-associated glomerulopathies.Nature reviews. Nephrology · 2016Review
- Timing of eculizumab therapy for C3 glomerulonephritis.Clinical kidney journal · 2015Article
- C3 Glomerulopathy and Atypical Hemolytic Uremic Syndrome: Two Important Manifestations of Complement System Dysfunction.Case reports in nephrology and dialysisArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundC3 glomerulonephritis (C3GN) is a rare form of glomerulopathy that is characterized by predominant C3 deposits. Eculizumab, a humanized monoclonal C5 antibody, has recently emerged as a treatment option for C3GN. We report a C3GN patient successfully treated with eculizumab. CASE DIAGNOSIS/TREATMENT: A 5-year-old boy who presented with proteinuria, hematuria, high ASO titers, and low C3 levels was initially diagnosed with post-streptococcal GN. His first kidney biopsy confirmed this diagnosis, but complement investigations identified three alternative pathway dysregulation factors: C3 nephritic factor, complement factor I heterozygous mutation (I398L), and anti-factor H autoantibodies (4,500 AU/ml). A second biopsy performed 11 months after initial presentation (nephrotic range proteinuria) showed a C3GN suggestive of isolated C3 deposits. Despite the use of intensive immunosuppressive therapy (rituximab, corticosteroids, mycophenolate), nephrotic-range proteinuria persisted and a third kidney biopsy showed the same C3GN pattern with more endocapillary proliferation. The serum C5b-9 level was elevated. Eculizumab was initiated and resulted in a significant decline of proteinuria (5.3 to 1.3 g/day) and an improvement in pathologic features. A transient interruption of eculizumab resulted in a rapid rise in proteinuria to 9.3 g/day, which decreased to 0.8 g/day after resumption of treatment.
conclusionsThe administration of anti-C5 antibodies may represent a valuable therapeutic option in patients with C3GN.
Indexed as
Identifiers
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.