ArticlePloS one2016
Podocyte Depletion in Thin GBM and Alport Syndrome.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Knowledge Mapping of Alport Syndrome: A Bibliometric Analysis From 2000 to 2025.Molecular genetics & genomic medicine · 2026Review
- Progressive Renal Dysfunction in Autosomal-dominant Alport Syndrome Co-occurring with C1q Nephropathy.Internal medicine (Tokyo, Japan) · 2025Article
- Decreased parietal epithelial cell density is linked to podocyte depletion and predictors of kidney disease progression in human kidneys.American journal of physiology. Renal physiology · 2025Article
- Collagen IV in Gould syndrome and Alport syndrome.Nature reviews. Nephrology · 2025Review
- Quantitative assessment of glomerular basement membrane collagen IV α chains in paraffin sections from patients with focal segmental glomerulosclerosis and Alport gene variants.Kidney international · 2024Article
- Review
- Role of detached podocytes in differentiating between minimal change disease and early focal segmental glomerulosclerosis, can we rely on routine light microscopy?Journal of nephrology · 2022Article
- A Systematic Review of PathogenicKidney international reports · 2022Article
- Heterozygous PathogenicKidney international reports · 2022Review
- Alport Syndrome With Kidney Cysts Is Still Alport Syndrome.Kidney international reports · 2022Article
- Guidelines for Genetic Testing and Management of Alport Syndrome.Clinical journal of the American Society of Nephrology : CJASN · 2022Article
- Genotype-Phenotype Correlations for PathogenicFrontiers in medicine · 2022Review
- PathogenicKidney360 · 2021Article
- Synaptopodin deficiency exacerbates kidney disease in a mouse model of Alport syndrome.American journal of physiology. Renal physiology · 2021Article
- Bidirectional, non-necrotizing glomerular crescents are the critical pathology in X-linked Alport syndrome mouse model harboring nonsense mutation of human COL4A5.Scientific reports · 2020Article
- Urinary podocyte mRNAs precede microalbuminuria as a progression risk marker in human type 2 diabetic nephropathy.Scientific reports · 2020Article
- Molecular and functional characterization of urine-derived podocytes from patients with Alport syndrome.The Journal of pathology · 2020Article
- Variations of type IV collagen-encoding genes in patients with histological diagnosis of focal segmental glomerulosclerosis.Pediatric nephrology (Berlin, Germany) · 2020Review
- Loss of Roundabout Guidance Receptor 2 (Robo2) in Podocytes Protects Adult Mice from Glomerular Injury by Maintaining Podocyte Foot Process Structure.The American journal of pathology · 2020Article
- Podocyte hypertrophic stress and detachment precedes hyperglycemia or albuminuria in a rat model of obesity and type2 diabetes-associated nephropathy.Scientific reports · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The proximate genetic cause of both Thin GBM and Alport Syndrome (AS) is abnormal α3, 4 and 5 collagen IV chains resulting in abnormal glomerular basement membrane (GBM) structure/function. We previously reported that podocyte detachment rate measured in urine is increased in AS, suggesting that podocyte depletion could play a role in causing progressive loss of kidney function. To test this hypothesis podometric parameters were measured in 26 kidney biopsies from 21 patients aged 2-17 years with a clinic-pathologic diagnosis including both classic Alport Syndrome with thin and thick GBM segments and lamellated lamina densa [n = 15] and Thin GBM cases [n = 6]. Protocol biopsies from deceased donor kidneys were used as age-matched controls. Podocyte depletion was present in AS biopsies prior to detectable histologic abnormalities. No abnormality was detected by light microscopy at <30% podocyte depletion, minor pathologic changes (mesangial expansion and adhesions to Bowman's capsule) were present at 30-50% podocyte depletion, and FSGS was progressively present above 50% podocyte depletion. eGFR did not change measurably until >70% podocyte depletion. Low level proteinuria was an early event at about 25% podocyte depletion and increased in proportion to podocyte depletion. These quantitative data parallel those from model systems where podocyte depletion is the causative event. This result supports a hypothesis that in AS podocyte adherence to the GBM is defective resulting in accelerated podocyte detachment causing progressive podocyte depletion leading to FSGS-like pathologic changes and eventual End Stage Kidney Disease. Early intervention to reduce podocyte depletion is projected to prolong kidney survival in AS.
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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.