Benazepril slows progression of renal dysfunction in patients with non-diabetic renal disease


Dr Toshihiko Ishimitsu, Department of Cardiovascular Medicine, Dokkyo Medical University, Mibu, Tochigi 321-0293, Japan. Email:


Aim:  The present study examined the effects of benazepril, an angiotensin-converting enzyme inhibitor, on the progression of renal insufficiency in patients with non-diabetic renal disease.

Methods:  Fifteen patients with non-diabetic renal disease whose serum creatinine (Cr) ranged from 1.5 to 3.0 mg/dL were given either benazepril (2.5–5 mg) or placebo once daily for 1 year in a random crossover manner. In both periods, antihypertensive medications were increased if blood pressure was greater than 130/85 mmHg. Blood sampling and urinalysis were performed bimonthly throughout the study period.

Results:  Blood pressure was similar when comparing the benazepril and the placebo periods (128 ± 12/83 ± 6 vs 129 ± 10/83 ± 7 mmHg). Serum Cr significantly increased from 1.62 ± 0.18 to 1.72 ± 0.30 mg/dL (P = 0.036) during the placebo period, while there was no statistically significant increase in serum Cr during the benazepril period (from 1.67 ± 0.17 to 1.71 ± 0.27 mg/dL). The slope of decrease of the reciprocal of serum Cr was steeper in the placebo period than in the benazepril period (−0.073 ± 0.067 vs−0.025 ± 0.096/year, P = 0.014). Urinary protein excretion was lower during the benazepril period than during the placebo period (0.57 ± 0.60 vs 1.00 ± 0.85 g/gCr, P = 0.006). Serum K was significantly higher in the benazepril period than in the placebo period (4.4 ± 0.5 vs 4.2 ± 0.5 mEq/L, P < 0.001), but no patient discontinued benazepril therapy as a result of hyperkalemia.

Conclusion:  Long-term benazepril treatment decreased the progression of renal dysfunction in patients with non-diabetic renal disease by a mechanism that is independent of blood pressure reduction.