Patients with stable renal insufficiency were randomized into two groups: (1) patients given the channel blocker nisoldipine (n = 17) and (2) placebo-treated patients (n = 17) also taking their regular antihypertensive therapy which did not include calcium blockers. Patients were already on low protein diet with a protein intake of 0.80 ± 0.2 in the nisoldipine group versus 0.85 ± 0.25 g/kg body weight in the placebo-treated group. The monthly progression of their renal failure was assessed by the reciprocal of serum creatinine versus time in months. After a mean follow-up of 17.4 ± 8.2 (range 6–30) months, the nisoldipine-treated group had a significant decrease in their slope of progression, whereas the placebo-treated patients, after 16.94 ± 7.2 (range 6–30) months of follow-up, had no significant change in their slope. The protein intake during follow-up was similar, being 0.85 ± 0.2 g/kg actual body weight in the nisoldipine-treated group and 0.88 ± 0.26 g/kg in the placebo group. The changes in slope did not correlate with the changes in blood pressure.

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Chronic renal failure (CRF) patients with a stable course were asked to participate in a follow-up program in which they were randomized into two groups: 1) the placebo group taking their standard antihypertensive therapy without any calcium ion blocker: and 2) the nisoldipine group, those patients taking the calcium channel blocker nisoldipine as the only antihypertensive drug. The two groups had similar blood pressures on entering the study (151 +/- 21.3/90.7 +/- 7.4 mmHg in the nisoldipine and 146.7 +/- 18/94 +/- 9.4 mmHg in the placebo group). Their protein intake was also similar (daily average throughout the follow-up period: 0.83 +/- 0.18 g protein per kg body weight in the nisoldipine and 0.9 +/- 0.12 g in the placebo group). The patients were checked monthly. The follow-up averaged 11.1 +/- 4.8 months in the nisoldipine group and 13.7 +/- 4.2 months in the placebo group. The rate of progression of CRF, as expressed by the slope of the regression line of 1/serum creatinine versus time, decreased in the nisoldipine group from the initial (-8.03 +/- 4.91) x 10(-3) to (-5.57 +/- 5) x 10(-3) (two-tailed P-test = 0.016) after intervention. The slopes tended to become steeper in the placebo group, with an initial slope of (-4.1 +/- 3.2) x 10(-3) changing to (-7.9 +/- 5) x 10(-3) after intervention. This difference did not reach statistical significance (two-tailed P = 0.072). The rate of progression of CRF decreased in 12 of 14 patients in the nisoldipine-treated group versus 3 of 11 patients in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)

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