ArticleKidney international2017
Accelerated podocyte detachment and progressive podocyte loss from glomeruli with age in Alport Syndrome.
Article in Kidney international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Potential Renal Damage Biomarkers in Alport Syndrome-A Review of the Literature.International journal of molecular sciences · 2022Pooled it
- New therapeutic hope for rare podocytopathies.Pediatric nephrology (Berlin, Germany) · 2026Review
- Decoding the urinary metabolome of aromatic amino acid pathways in Alport syndrome.Analytical and bioanalytical chemistry · 2026Article
- Glomage: A Multimodal Platform for High-Content Morphological and RNA Profiling of Glomeruli in Zebrafish and Mouse Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Knowledge Mapping of Alport Syndrome: A Bibliometric Analysis From 2000 to 2025.Molecular genetics & genomic medicine · 2026Review
- Podometrics as a translational platform for kidney health and disease: Oshima award address 2025.Clinical and experimental nephrology · 2026Review
- SPARC upregulation mediates podocyte injury in Alport syndrome mice.BMC nephrology · 2026Article
- WNK1 Kinase Activity Is Required for the Functional Maintenance of Podocyte Structure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Urinary Podocyte Loss is Associated With Treatment Response in Patients With Primary Nephrotic Syndrome.Kidney international reports · 2026Article
- Slight acceleration in podocyte mRNA loss in preterm-born children aged 3-5 years.Pediatric nephrology (Berlin, Germany) · 2026Article
- The role of endothelin receptor antagonists in kidney disease.Renal failure · 2025Review
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- Lipidomics Unveils Critical Lipid Pathway Shifts in Alport Syndrome.Kidney international reports · 2025Article
- Increased urinary podocyte mRNA loss in healthy early-term infants.Pediatric nephrology (Berlin, Germany) · 2025Article
- A novel mouse model for X-linked Alport syndrome induced by splicing mutation in the Col4a5 gene.Scientific reports · 2025Article
- Biomarkers for the early diagnosis of Alport syndrome and associated kidney damage.Childhood kidney diseases · 2025Review
- Ezetimibe Enhances Lipid Droplet and Mitochondria Contact Formation, Improving Fatty Acid Transfer and Reducing Lipotoxicity in Alport Syndrome Podocytes.International journal of molecular sciences · 2024Article
- Advancing the application of the analytical renal pathology system in allograft IgA nephropathy patients.Renal failure · 2024Article
- Urinary podocyte markers of disease activity, therapeutic efficacy, and long-term outcomes in acute and chronic kidney diseases.Clinical and experimental nephrology · 2024Review
- Podocyte involvement in the pathogenesis of preterm-related long-term chronic kidney disease.Histology and histopathology · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Podocyte depletion is a common mechanism driving progression in glomerular diseases. Alport Syndrome glomerulopathy, caused by defective α3α4α5 (IV) collagen heterotrimer production by podocytes, is associated with an increased rate of podocyte detachment detectable in urine and reduced glomerular podocyte number suggesting that defective podocyte adherence to the glomerular basement membrane might play a role in driving progression. Here a genetically phenotyped Alport Syndrome cohort of 95 individuals [urine study] and 41 archived biopsies [biopsy study] were used to test this hypothesis. Podocyte detachment rate (measured by podocin mRNA in urine pellets expressed either per creatinine or 24-hour excretion) was significantly increased 11-fold above control, and prior to a detectably increased proteinuria or microalbuminuria. In parallel, Alport Syndrome glomeruli lose an average 26 podocytes per year versus control glomeruli that lose 2.3 podocytes per year, an 11-fold difference corresponding to the increased urine podocyte detachment rate. Podocyte number per glomerulus in Alport Syndrome biopsies is projected to be normal at birth (558/glomerulus) but accelerated podocyte loss was projected to cause end-stage kidney disease by about 22 years. Biopsy data from two independent cohorts showed a similar estimated glomerular podocyte loss rate comparable to the measured 11-fold increase in podocyte detachment rate. Reduction in podocyte number and density in biopsies correlated with proteinuria, glomerulosclerosis, and reduced renal function. Thus, the podocyte detachment rate appears to be increased from birth in Alport Syndrome, drives the progression process, and could potentially help predict time to end-stage kidney disease and response to treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.