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Renal Allograft Protection with Angiotensin II Type 1 Receptor Antagonists
Article first published online: 7 NOV 2006
DOI: 10.1111/j.1600-6143.2006.01588.x
Additional Information
How to Cite
Tylicki, L., Biedunkiewicz, B., Chamienia, A., Wojnarowski, K., Zdrojewski, Z., Aleksandrowicz, E., Lysiak-Szydlowska, W. and Rutkowski, B. (2007), Renal Allograft Protection with Angiotensin II Type 1 Receptor Antagonists. American Journal of Transplantation, 7: 243–248. doi: 10.1111/j.1600-6143.2006.01588.x
Publication History
- Issue published online: 7 NOV 2006
- Article first published online: 7 NOV 2006
- Received 8 February 2006, revised 7 September 2006 and accepted for publication 8 September 2006
- Abstract
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Keywords:
- Angiotensin receptor blocker;
- chronic allograft nephropathy;
- fibrosis;
- losartan;
- renal transplant recipients;
- tubules
In 16 renal transplant recipients in this randomized trial, losartin decreased urinary proteins associated with renal damage compared with a beta blocker.
The renal benefits of agents inhibiting the renin-angiotensin-aldosterone system in renal transplant recipients, i.e. preventing the development of chronic graft nephropathy, are supposed but not finally proven. In a double-blind, placebo-controlled, cross-over study, we evaluated the influence of losartan on surrogate markers of tubular injury, urine excretion of transforming growth factor β-1 (TGF-β1) and amino-terminal propeptide of type III procollagen (PIIINP) in 16 patients after transplantation. The patients received randomly either losartan (50–100 mg daily) or the β-blocker carvedilol (12.5–25 mg) for 8 weeks, allowing a placebo washout between treatments. The target office through blood pressure (BP) was below 130/85 mmHg. The BP did not differ in the treatment periods. Losartan significantly decreased N-acetyl-β-d-glucosaminidase and alfa-1 microglobulin excretion relative to placebo and carvedilol. Urine excretion of TGF-β1 and PIIINP was significantly lower after losartan. In conclusion, losartan reduces urine excretion of proteins associated with tubular damage and graft fibrosis.