Effects of valsartan on the progression of chronic renal insufficiency in patients with nondiabetic renal diseases

Toshihiko Ishimitsu, Tomoko Kameda, Akira Akashiba, Toshiaki Takahashi, Norikazu Ando, Satoshi Ohta, Masayoshi Yoshii, Hideki Inada, Kohju Tsukada, Junichi Minami, Hidehiko Ono, Hiroaki Matsuoka
Hypertension Research: Official Journal of the Japanese Society of Hypertension 2005, 28 (11): 865-70
The present study tested the effects of valsartan, an angiotensin II receptor blocker, on the progression of renal insufficiency in patients with nondiabetic renal diseases. The study subjects were 22 patients with nondiabetic renal diseases whose serum creatinine (Cr) ranged from 1.5 to 3.0 mg/dl. Valsartan (40-80 mg) or placebo was given once daily for 1 year each in a random crossover manner. In both periods, antihypertensive medications were titrated when the blood pressure was not lower than 140/90 mmHg. Blood sampling and urinalysis were performed bimonthly throughout the study periods. The average blood pressure was comparable between the valsartan and the placebo periods (130 +/- 9/86 +/- 6 vs. 131 +/- 8/86 +/- 6 mmHg). Serum Cr significantly increased from 1.9 +/- 0.5 to 2.3 +/- 0.8 mg/dl (p < 0.001) during the placebo period, but the change was insignificant in the valsartan period (2.1 +/- 0.6 to 2.2 +/- 0.9 mg/dl). The slope of decrease in the reciprocal of serum Cr was steeper in the placebo period than in the valsartan period (-0.064 +/- 0.070/year vs. -0.005 +/- 0.050/year, p < 0.01). During the valsartan period, urinary protein excretion was less than that during the placebo period (0.75 +/- 0.73 vs. 1.24 +/- 0.92 g/g Cr, p < 0.001). Serum K was significantly higher in the valsartan period than in the placebo period (4.6 +/- 0.5 vs. 4.4 +/- 0.5 mEq/l, p < 0.05); however, no patients discontinued taking valsartan as a result of hyperkalemia. It is possible that long-term treatment with an angiotensin II receptor blocker, valsartan, is effective at retarding the deterioration of renal function in patients with nondiabetic renal disease by a mechanism independent of blood pressure reduction.

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