Key result
Valsartan significantly slowed the decline in renal function compared to placebo, as measured by the slope of the reciprocal of serum creatinine (-0.005 vs -0.064/year, p<0.01).
Why the study?
Does valsartan reduce the progression of renal insufficiency in patients with nondiabetic renal diseases?
RCT (n=22)
Single-blind
Random crossover
No
Does valsartan reduce the progression of renal insufficiency in patients with nondiabetic renal diseases?
Valsartan effectively retards the deterioration of renal function and reduces urinary protein excretion in patients with nondiabetic renal disease, independent of blood pressure reduction.
Supports valsartan to slow renal decline in nondiabetic CKD; extends renoprotection evidence beyond diabetes.
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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Ishimitsu et al. (2005) conducted an RCT in Nondiabetic renal diseases with chronic renal insufficiency (n=22). Valsartan vs. Placebo was evaluated on Slope of time-course changes in the reciprocal of serum creatinine (1/Cr) per year (p=<0.01). Valsartan significantly slowed the decline in renal function compared to placebo, as measured by the slope of the reciprocal of serum creatinine (-0.005 vs -0.064/year, p<0.01).
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