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TGF-beta1 mRNA upregulation influences chronic renal allograft dysfunction
P Pribylova-Hribova1, K Kotsch, A Lodererova
1Transplant Laboratory, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. petra.hribova@medicon.cz
Kidney International
|April 14, 2006
Summary
Transforming growth factor-beta1 (TGF-beta1) is elevated in kidney transplant rejection and dysfunction. This key molecule may play a significant role in chronic allograft nephropathy development.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Acute rejection (AR) is a major risk factor for chronic allograft nephropathy (CAN) after kidney transplantation.
- CAN involves progressive interstitial fibrosis and is linked to increased transforming growth factor-beta1 (TGF-beta1) expression, but its kinetics remain unclear.
Purpose of the Study:
- To investigate the role of intragraft TGF-beta1 expression in early graft dysfunction and its influence on late renal allograft dysfunction.
Main Methods:
- Quantified TGF-beta1 mRNA expression in 174 human renal biopsies using real-time reverse transcriptase-polymerase chain reaction.
- Correlated expression levels with Banff histopathological grades, TGF-beta1 immunohistology, and clinical outcomes.
Main Results:
- TGF-beta1 was significantly upregulated in AR, CAN, and acute tubular necrosis with delayed graft function compared to controls.
- Heightened TGF-beta1 expression was observed in borderline changes, recurrent glomerulonephritis, and cyclosporine toxicity.
- TGF-beta1 overexpression in CAN correlated with an increased risk of renal allograft dysfunction at 18 months.
Conclusions:
- Intragraft TGF-beta1 mRNA expression is significantly upregulated in both AR and CAN.
- These findings support a key role for TGF-beta1 in the pathogenesis of chronic allograft dysfunction.
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