ArticlePediatric nephrology (Berlin, Germany)2020
Treatment-resistant nephrotic syndrome in dense deposit disease: complement-mediated glomerular capillary wall injury?
Article in Pediatric nephrology (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 2 citations in OpenAlex.
- Favorable outcome in children with dense deposit disease with the use of long-term mycophenolate mofetil and high-dose alternate-day steroids.Pediatric nephrology (Berlin, Germany) · 2025Article
- Repository Corticotropin in Treating de novo C3 Glomerulonephritis after Transplantation.Glomerular diseases · 2022Article
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5 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe C3 glomerulopathies (C3G) are recently defined glomerular diseases, attributed to abnormal complement regulation. Dense deposit disease (DDD) is part of the spectrum of C3G, characterized by electron-dense deposits in the lamina densa of the glomerular basement membrane. Patients with DDD present with hematuria, variable degrees of proteinuria, and kidney dysfunction. Kidney biopsies typically disclose proliferative and inflammatory patterns of injury. Treatment with glucocorticoids and mycophenolate mofetil has been shown to achieve remission of proteinuria in a significant proportion of C3G patients. CASE-DIAGNOSIS/TREATMENT: We report two patients with persistent nephrotic syndrome while on immunosuppressive therapy. Repeat kidney biopsies disclosed massive C3 deposits with foot process effacement in the absence of proliferative or inflammatory lesions on light microscopy.
conclusionThese cases, coupled with data from animal models of disease and the variable response to eculizumab in C3G patients, illustrate that two different pathways might be involved in the development of kidney injury in C3G: a C5-independent pathway leading to glomerular capillary wall injury and the development of proteinuria versus a C5-dependent pathway that causes proliferative glomerulonephritis and kidney dysfunction.
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