ArticlePediatric nephrology (Berlin, Germany)2011
Minimal change disease: a "two-hit" podocyte immune disorder?
Article in Pediatric nephrology (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 117 citations in OpenAlex.
- Association between anti-nephrin autoantibodies and disease activity in minimal change disease.Annals of medicine · 2026Article
- Nephrotic Syndrome: Current Management.Indian journal of pediatrics · 2026Review
- Effects of TNF-α, IL-1β and IL-2 on regulatory T cells in children with idiopathic nephrotic syndrome.Frontiers in pediatrics · 2026Article
- Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.Clinical kidney journal · 2026Review
- Immune checkpoint inhibitor-induced nephrotic syndrome: a pharmacovigilance analysis of 404 FAERS cases and literature case series.Renal failure · 2025Article
- Immune Checkpoint Signatures in Minimal Change Disease and Membranous Nephropathy: Divergent Pathways of a Shared Imbalance.International journal of molecular sciences · 2025Article
- Isolated superior mesenteric vein thrombosis in an adult with nephrotic syndrome due to minimal change disease: a case report.Journal of medical case reports · 2025Article
- Article
- The Role of TNF-α in the Pathogenesis of Idiopathic Nephrotic Syndrome and Its Usefulness as a Marker of the Disease Course.Journal of clinical medicine · 2024Article
- Exploration of the pathogenesis of nephrotic syndrome and traditional Chinese medicine intervention based on gut microbiota.Frontiers in immunology · 2024Review
- The role of toll-like receptors (TLRs) and their therapeutic applications in glomerulonephritis.International urology and nephrology · 2023Review
- Incidence of idiopathic nephrotic syndrome during the Covid-19 pandemic in the Paris area (France) and in the Netherlands.Pediatric nephrology (Berlin, Germany) · 2023Article
- Age of Onset and Disease Course in Biopsy-Proven Minimal Change Disease: An Analysis From the Cure Glomerulonephropathy Network.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2023Observational
- Preliminary study of anti-CD40 and ubiquitin proteasome antibodies in primary podocytopaties.Frontiers in medicine · 2023Article
- Second and Third Generational Advances in Therapies of the Immune-Mediated Kidney Diseases in Children and Adolescents.Children (Basel, Switzerland) · 2022Review
- New Insights into the Treatment of Glomerular Diseases: When Mechanisms Become Vivid.International journal of molecular sciences · 2022Review
- Significance of regulatory T cells in children with idiopathic nephrotic syndrome.Journal of nephrology · 2022Article
- Spectrum of Kidney Injury Following COVID-19 Disease: Renal Biopsy Findings in a Single Italian Pathology Service.Biomolecules · 2022Article
- Serum IL-12p40: A novel biomarker for early prediction of minimal change disease relapse following glucocorticoids therapy.Frontiers in medicine · 2022Article
- The role of the immune system in idiopathic nephrotic syndrome.Molecular and cellular pediatrics · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Minimal change disease (MCD) is the most common nephrotic syndrome in children and is commonly thought to be a T-cell disorder mediated by a circulating factor that alters podocyte function resulting in massive proteinuria. We suggest that MCD is a "two-hit" disorder. As originally hypothesized by Reiser et al. in 2004, we propose that the initial hit is the induction of CD80 (also known as B7.1) on the podocyte, and that this results in an alteration in shape with actin rearrangement that alters glomerular permeability and causes proteinuria. We propose that CD80 expression may result from either direct binding of the podocyte by cytokines from activated T cells or by activation of podocyte toll-like receptors (TLR) by viral products or allergens. We further hypothesize that under normal circumstances, CD80 expression is only transiently expressed and proteinuria is minimal due to rapid autoregulatory response by circulating T regulatory cells or by the podocyte itself, probably due to the expression of factors [cytotoxic T-lymphocyte-associated (CTLA)-4, interleukin (IL)-10, and possibly transforming growth factor (TGF)-β] that downregulate the podocyte CD80 response. In MCD, however, there is a defect in CD80 podocyte autoregulation. This results in persistent CD80 expression and persistent proteinuria. If correct, this hypothesis may lead to both new diagnostic tests and potential therapeutics for this important renal disease.
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