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Renal Allograft Protection with Angiotensin II Type 1 Receptor Antagonists
Author(s) -
Tylicki L.,
Biedunkiewicz B.,
Chamienia A.,
Wojnarowski K.,
Zdrojewski Z.,
Aleksandrowicz E.,
LysiakSzydlowska W.,
Rutkowski B.
Publication year - 2007
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2006.01588.x
Subject(s) - losartan , medicine , excretion , endocrinology , transplantation , carvedilol , chronic allograft nephropathy , urology , angiotensin ii , nephropathy , blood pressure , kidney transplantation , heart failure , diabetes mellitus
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.