ReviewInternational journal of molecular sciences2024
Detailed Pathophysiology of Minimal Change Disease: Insights into Podocyte Dysfunction, Immune Dysregulation, and Genetic Susceptibility.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Genetic mutation patterns in Indonesian children with primary steroid-resistant nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2026Article
- Heparanase inhibition prevents glycocalyx damage and albuminuria in experimental minimal change disease.Clinical and translational medicine · 2026Article
- Role of LONP1 in human diseases: molecular mechanisms and therapeutic potential.Cellular & molecular biology letters · 2026Review
- miRNAs in Glomerular Diseases: From Pathogenic Insight to Therapeutic Potential: A Narrative Review.Cells · 2026Review
- An exploratory analysis of disulfidptosis-related gene signatures in minimal change disease identifies metabolic and immune associations.Frontiers in cell and developmental biology · 2026Article
- When Minimal Becomes Massive: A Case Report of Childhood-Onset Minimal Change Disease Marching to End Stage Renal Disease Despite Modern Immunotherapy.Clinical medicine insights. Case reports · 2026Article
- Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.Clinical kidney journal · 2026Review
- Immune Checkpoint Signatures in Minimal Change Disease and Membranous Nephropathy: Divergent Pathways of a Shared Imbalance.International journal of molecular sciences · 2025Article
- Review
- Nicotinism vs. Glomerulopathies-Smoking as a Risk Factor for Primary Glomerulopathies.Antioxidants (Basel, Switzerland) · 2025Review
- Patterns of Glomerular Injury: Histopathological Classification and Clinical Correlation.Cureus · 2025Review
- Shared hub genes in membranous nephropathy and kidney renal clear cell carcinoma: investigating molecular overlap and tumor progression.Discover oncology · 2025Article
- How to identify IgA nephropathy presenting as nephrotic syndrome coexisting with minimal change disease? A 15-year single-center clinicopathological analysis.Frontiers in immunology · 2025Article
- Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Minimal Change Disease (MCD) is a predominant cause of idiopathic nephrotic syndrome in the pediatric population, yet presents significant clinical challenges due to its frequent relapses and steroid resistance. Despite its relatively benign histological appearance, MCD is characterized by severe proteinuria, hypoalbuminemia, and edema, which may affect patient outcomes. Current treatment strategies primarily rely on corticosteroids, which are effective in inducing remission but are associated with high relapse rates, steroid resistance, and numerous long-term side effects, underscoring the need for more targeted and effective therapeutic approaches. This narrative review synthesizes current knowledge on the pathophysiological mechanisms underlying MCD, focusing on the following three critical areas: podocyte dysfunction, immune dysregulation, and genetic susceptibility. Podocyte dysfunction, particularly involving alterations in nephrin, plays a central role in the breakdown of the glomerular filtration barrier, leading to the characteristic proteinuria observed in MCD. Immune dysregulation, including the presence of autoantibodies against nephrin and other podocyte components, exacerbates podocyte injury and contributes to disease progression, suggesting an autoimmune component to the disease. Genetic factors, particularly mutations in the NPHS1 and NPHS2 genes, have been identified as significant contributors to disease susceptibility, influencing the variability in treatment response and overall disease severity. Understanding these mechanisms is crucial for developing targeted therapies that address the underlying causes of MCD rather than merely managing its symptoms. This review highlights the need for further research into these pathophysiological processes to pave the way for more personalized and effective treatment strategies, ultimately improving patient outcomes and reducing reliance on corticosteroids.
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