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Updated: Jun 10, 2026
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Epithelial Cell Repopulation and Preparation of Rodent Extracellular Matrix Scaffolds for Renal Tissue Development
Published on: August 10, 2015
[Epithelial-mesenchymal transition in kidney grafts]
Eric Rondeau1, Alexandre Hertig, Cédric Rafat
1Urgences Néphrologiques et Transplantation rénale, et INSERM UMRS 702, Hôpital Tenon, 4 rue de la Chine, 75020 Paris. eric.rondeau@tnn.aphp.fr
Bulletin De L'Academie Nationale De Medecine
|July 30, 2010
Summary
Kidney graft fibrosis, a cause of graft loss, involves epithelial-mesenchymal transition. Early detection of these changes predicts fibrosis and poorer long-term kidney function, suggesting therapeutic targets.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Context:
- Late kidney graft loss is primarily caused by progressive sclerosis.
- Fibrosis involves immune and non-immune processes, including epithelial-mesenchymal transition (EMT).
- EMT is a mechanism where tubular epithelial cells gain mesenchymal traits, contributing to fibrosis.
Purpose:
- To investigate the presence and implications of EMT in kidney grafts.
- To determine if early EMT markers predict fibrosis and graft function.
- To explore the association between EMT, ischemia, rejection, and graft outcomes.
Summary:
- Immunohistochemistry revealed tubular epithelial cells in kidney grafts exhibit EMT markers as early as 3 months post-transplantation.
- These early EMT changes correlate with prolonged cold ischemia and acute rejection.
- EMT markers at 3 months predict fibrosis at 12 months and its progression, as well as poorer renal function at 2 years.
Impact:
- EMT is an early event in kidney graft fibrosis.
- Early identification of EMT could serve as a predictive biomarker for graft outcomes.
- Targeting EMT may offer a strategy to prevent fibrosis and preserve renal function, reducing late graft loss.
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