ReviewKidney diseases (Basel, Switzerland)2020
Mechanisms of Podocyte Detachment, Podocyturia, and Risk of Progression of Glomerulopathies.
Review in Kidney diseases (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Reduced podocyte stiffness is a feature of proteinuric kidney disease.Kidney international · 2026Article
- The urinary albumin-to-creatinine ratio can direct personalized prevention and treatment for cardiovascular and chronic kidney disease.Journal of internal medicine · 2026Review
- Clinical Determinants of Urinary Podocyte Biomarkers and Their Feasibility in Paraprotein-Related Kidney Disease.Diagnostics (Basel, Switzerland) · 2026Article
- Article
- Pathogenic mechanisms in Fabry disease.Frontiers in medicine · 2026Review
- Cage-Farming Causes Histopathological Alterations in the Renal Tissues of the Rainbow TroutInternational journal of molecular sciences · 2025Article
- Fabry Disease Beyond Storage: The Role of Inflammation in Disease Progression.International journal of molecular sciences · 2025Review
- From fat to filter: the effect of adipose tissue-derived signals on kidney function.Nature reviews. Nephrology · 2025Review
- Finerenone: Potential Clinical Application Across the Spectrum of Cardiovascular Disease and Chronic Kidney Disease.Journal of clinical medicine · 2025Review
- Podocyturia an emerging biomarker for kidney injury.BMC nephrology · 2025Review
- Chitosan nanoencapsulation of Turbinaria triquetra metabolites in the management of podocyturia in nephrotoxic rats.Scientific reports · 2025Article
- The Kidney in Obesity: Current Evidence, Perspectives and Controversies.Current obesity reports · 2024Review
- Roles of myosin 1e and the actin cytoskeleton in kidney functions and familial kidney disease.Cytoskeleton (Hoboken, N.J.) · 2024Review
- INF2 formin variants linked to human inherited kidney disease reprogram the transcriptome, causing mitotic chaos and cell death.Cellular and molecular life sciences : CMLS · 2024Article
- Characterizing Glomerular Barrier Dysfunction with Patient-Derived Serum in Glomerulus-on-a-Chip Models: Unveiling New Insights into Glomerulonephritis.International journal of molecular sciences · 2024Article
- The role of tubular cells in the pathogenesis of Fabry nephropathy.Frontiers in cardiovascular medicine · 2024Review
- Profilin1 is required for prevention of mitotic catastrophe in murine and human glomerular diseases.The Journal of clinical investigation · 2023Article
- PFKFB3 downregulation aggravates Angiotensin II-induced podocyte detachment.Renal failure · 2023Article
- Nanoparticle Tracking Analysis of Urinary Extracellular Vesicle Proteins as a New Challenge in Laboratory Medicine.International journal of molecular sciences · 2023Article
- Advancing drug discovery for glomerulopathies using stem-cell-derived kidney models.Trends in pharmacological sciences · 2023Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlomerulopathies are the main cause of ESRD. Primary or secondary causes of glomerular diseases comprise more than 70% of cases that end up in renal replacement therapies. SUMMARY: The total glomerular mass that each individual contains is key to maintaining normal kidney function. Diabetes, hypertension, and any primary or secondary glomerulopathy may threaten the normal glomerular function. In fact, any glomerular insult may alter the glomerular filtration barrier, which in turn is composed by the podocyte, the glomerular basement membrane, and the capillary endothelial cell. Deposition of immune complexes, antibodies, or complement components at the subepithelial, intramembranous, or subendothelial space, and mutations in podocyte, slit diaphragm, or glomerular basement membrane proteins or enzymes are the main etiologies of glomerular alterations. Podocytes are glomerular cells that do not divide under normal circumstances. In this respect, maintenance of the absolute podocyte number per glomer-ulus is critical for normal glomerular function. As the insult progresses, podocytes start to detach from the glomerular basement membrane. When the podocyte loss is over 40% in a glomerulus, glomerulosclerosis develops, and obliteration of the glomerulus is the rule. In clinical grounds, this phenomenon is diagnosed mainly by proteinuria and a decline in glomerular filtration rate. KEY MESSAGES: In this review article, the impact of podocyturia in glomerular diseases and the main mechanisms of podocyte detachment are discussed. Finally, potential targets of therapeutic approach are suggested.
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