ArticleClinical kidney journal2018
Membranoproliferative glomerulonephritis and C3 glomerulopathy in children: change in treatment modality? A report of a case series.
Article in Clinical kidney journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Complement-targeted therapies for C3 glomerulopathy and atypical hemolytic uremic syndrome: a time-limited rapid systematic review with narrative synthesis.Frontiers in medicine · 2026Review
- To biopsy or not to biopsy a teenager with idiopathic nephrotic syndrome? Biopsy first.Pediatric nephrology (Berlin, Germany) · 2025Article
- Long-term follow-up including extensive complement analysis of a pediatric C3 glomerulopathy cohort.Pediatric nephrology (Berlin, Germany) · 2022Article
- Characteristics and outcomes of glomerulonephritis with membranoproliferative pattern in children.Translational pediatrics · 2021Article
- The newClinical kidney journal · 2019Article
- Recurrent andFrontiers in immunology · 2019Review
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Authors and funding
9 authors.
Funding
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Abstract
backgroundMembranoproliferative glomerulonephritis (MPGN) with immune complexes and C3 glomerulopathy (C3G) in children are rare and have a variable outcome, with some patients progressing to end-stage renal disease (ESRD). Mutations in genes encoding regulatory proteins of the alternative complement pathway and of complement C3 (C3) have been identified as concausative factors.
methodsThree children with MPGN type I, four with C3G, i.e. three with C3 glomerulonephritis (C3GN) and one with dense deposit disease (DDD), were followed. Clinical, autoimmune data, histological characteristics, estimated glomerular filtration rate (eGFR), proteinuria, serum C3, genetic and biochemical analysis were assessed.
resultsThe median age at onset was 7.3 years and the median eGFR was 72 mL/min/1.73 m
conclusionsIn children with MPGN type I and C3G, the outcomes of renal function and response to treatment modality show great variability independent from histological diagnosis at disease onset. In case of severe clinical presentation at disease onset, early genetic and biochemical analysis of the alternative pathway dysregulation is recommended. Treatment with eculizumab appears to be an option to slow disease progression in single cases.
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