ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2017
Urinary podocyte and TGF-β1 mRNA as markers for disease activity and progression in anti-glomerular basement membrane nephritis.
Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 17 citations in OpenAlex.
- Sodium-glucose cotransporter 2 inhibitor ameliorates podocyte hypertrophic stress by suppressing the mTOR/p70S6K/cyclin D1 signaling pathway in obesity-related nephropathy.Scientific reports · 2026Article
- Continuous increase in podocyte numbers in the first 36 months of life-insights from forensic autopsies in Japanese children.Pediatric nephrology (Berlin, Germany) · 2025Article
- Urinary podocyte markers of disease activity, therapeutic efficacy, and long-term outcomes in acute and chronic kidney diseases.Clinical and experimental nephrology · 2024Review
- Urinary podocyte markers in diabetic kidney disease.Kidney research and clinical practice · 2024Article
- Circulating Nucleic Acid-Based Biomarkers of Type 2 Diabetes.International journal of molecular sciences · 2021Review
- Urinary mRNA Expression of Glomerular Podocyte Markers in Glomerular Disease and Renal Transplant.Diagnostics (Basel, Switzerland) · 2021Article
- Associations between the concentrations of CD68, TGF-β1, renal injury index and prognosis in glomerular diseases.Experimental and therapeutic medicine · 2020Article
- Urinary podocyte mRNAs precede microalbuminuria as a progression risk marker in human type 2 diabetic nephropathy.Scientific reports · 2020Article
- Urinary podocyte mRNA is a potent biomarker of anti-neutrophil cytoplasmic antibody-associated glomerulonephritis.Clinical and experimental nephrology · 2020Article
- Podocyte hypertrophic stress and detachment precedes hyperglycemia or albuminuria in a rat model of obesity and type2 diabetes-associated nephropathy.Scientific reports · 2019Article
- Quercetin suppresses glomerulosclerosis and TGF‑β signaling in a rat model.Molecular medicine reports · 2019Article
- Accelerated podocyte detachment and progressive podocyte loss from glomeruli with age in Alport Syndrome.Kidney international · 2017Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPodocyte depletion causes glomerulosclerosis, with persistent podocyte loss being a major factor driving disease progression. Urinary podocyte mRNA is potentially useful for monitoring disease progression in both animal models and in humans. To determine whether the same principles apply to crescentic glomerular injury, a rat model of anti-glomerular basement membrane (anti-GBM) nephritis was studied in parallel with a patient with anti-GBM nephritis.
methodsPodocyte loss was measured by Wilms' Tumor 1-positive podocyte nuclear counting and density, glomerular epithelial protein 1 or synaptopodin-positive podocyte tuft area and urinary podocyte mRNA excretion rate. Glomerulosclerosis was evaluated by Azan staining and urinary transforming growth factor (TGF)-β1 mRNA excretion rate.
resultsIn the rat model, sequential kidney biopsies revealed that after a threshold of 30% podocyte loss, the degree of glomerulosclerosis was linearly associated with the degree of podocyte depletion, compatible with podocyte depletion driving the sclerotic process. Urinary podocyte mRNA correlated with the rate of glomerular podocyte loss. In treatment studies, steroids prevented glomerulosclerosis in the anti-GBM model in contrast to angiotensin II inhibition, which lacked a protective effect, and urinary podocyte and TGF-β1 mRNA markers more accurately reflected both the amount of podocyte depletion and the degree of glomerulosclerosis compared with proteinuria under both scenarios. In a patient successfully treated for anti-GBM nephritis, urinary podocyte and TGB-β1 mRNA reflected treatment efficacy.
conclusionThese results emphasize the role of podocyte depletion in anti-GBM nephritis and suggest that urinary podocyte and TGF-β1 mRNA could serve as markers of disease progression and treatment efficacy.
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