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Updated: Jul 8, 2026
17:13
Non-invasive Imaging of Acute Allograft Rejection after Rat Renal Transplantation Using 18F-FDG PET
Published on: April 28, 2013
Acute rejection modulates gene expression in the collecting duct
Bayram Edemir1, Stefan Reuter, Reka Borgulya
1Medizinische Klinik und Poliklinik D, Experimentelle Nephrologie, Domagkstrasse 3a, 48149 Münster, Germany. edemir@uni-muenster.de
Journal of the American Society of Nephrology : JASN
|January 25, 2008
Summary
Kidney transplant rejection alters gene expression, impairing kidney function by downregulating water and solute transporters. Cyclosporine A treatment preserves some transporter function, improving solute and water regulation.
Area of Science:
- Nephrology
- Molecular Biology
- Transplantation Immunology
Background:
- Kidney transplantation can lead to acute rejection, affecting graft function.
- Changes in gene expression, particularly for transporters, are implicated in post-transplant dysfunction.
Purpose of the Study:
- To investigate the impact of acute rejection on gene expression of renal transporters.
- To determine the role of rejection in the downregulation of water and solute channels.
- To assess the effect of cyclosporine A on transporter gene expression and kidney function.
Main Methods:
- Utilized a rat model of allogeneic renal transplantation with acute rejection.
- Performed gene array analysis to assess transporter expression.
- Compared gene expression in allogeneic vs. syngeneic transplantation and with cyclosporine A treatment.
Main Results:
- Acute rejection impaired renal function and downregulated aquaporins (water channels) and solute transporters.
- Syngeneic transplantation or cyclosporine A treatment partially prevented transporter downregulation.
- Rejection-dependent downregulation was observed for aquaporin-2 and epithelial sodium channel.
Conclusions:
- Altered gene expression of renal transporters contributes to impaired solute and water handling post-transplantation, especially during acute rejection.
- Cyclosporine A improves solute and water regulation by preserving aquaporin-2 and epithelial sodium channel expression, despite other transporter downregulation.
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