M Nowicki1, G Szewczyk-Seifert, D Klimek, F Kokot. 1. Department of Nephrology, Endocrinology and Metabolic Diseases, Silesian University School of Medicine, Katowice, Poland. nefro@wp.pl
Abstract
BACKGROUND AND AIM: Non-selective beta-adrenergic blockers may cause hyperkalemia in patients with end-stage renal failure. In contrast, alpha-adrenergic blockade has been found to decrease the hyperkalemic effect of physical exercise in healthy subjects, although we were unable to confirm this effect in hemodialysis patients. In a crossover design, we studied the effect of carvedilol, a non-selective beta-adrenergic blocker with an additional alpha1-blocking activity, on exercise-induced hyperkalemia in 17 anuric hemodialysis patients. METHODS: All subjects were given either carvedilol (25 mg/day) or placebo for 2 weeks in a random order with a 2-week wash-out period. At the end of each treatment period they underwent a 30-minute exercise test on a bicycle ergometer with a fixed load of 20 W. RESULTS: The treatment with carvedilol caused a significant decrease in blood pressure. Serum potassium before exercise tests was similar (5.37 +/- 0.2 and 5.24 +/- 0.2 mmol/l on carvedilol and placebo, respectively; mean +/- SE). During the exercise, serum potassium increased significantly (p < 0.001 in both tests) and subsequently decreased during 30 minutes of recovery (p < 0.05). The mean rate of potassium increment during the exercise was similar (23.3 +/- 3.3 micromol/l/min on carvedilol and 20.0 +/- 3.6 micromol/l/min on placebo). During recovery, the mean rate of potassium decrement was 5.0 +/- 3.0 micromol/l/min and 6.7 +/- 2.7 micromol/l/min, respectively. Serum sodium, ionized calcium, insulin and plasma renin activity were similar before the exercise tests and did not change during the exercise. CONCLUSION:Carvedilol does not enhance the hyperkalemic effect of moderate physical exercise in anuric hemodialysis patients.
RCT Entities:
BACKGROUND AND AIM: Non-selective beta-adrenergic blockers may cause hyperkalemia in patients with end-stage renal failure. In contrast, alpha-adrenergic blockade has been found to decrease the hyperkalemic effect of physical exercise in healthy subjects, although we were unable to confirm this effect in hemodialysis patients. In a crossover design, we studied the effect of carvedilol, a non-selective beta-adrenergic blocker with an additional alpha1-blocking activity, on exercise-induced hyperkalemia in 17 anuric hemodialysis patients. METHODS: All subjects were given either carvedilol (25 mg/day) or placebo for 2 weeks in a random order with a 2-week wash-out period. At the end of each treatment period they underwent a 30-minute exercise test on a bicycle ergometer with a fixed load of 20 W. RESULTS: The treatment with carvedilol caused a significant decrease in blood pressure. Serum potassium before exercise tests was similar (5.37 +/- 0.2 and 5.24 +/- 0.2 mmol/l on carvedilol and placebo, respectively; mean +/- SE). During the exercise, serum potassium increased significantly (p < 0.001 in both tests) and subsequently decreased during 30 minutes of recovery (p < 0.05). The mean rate of potassium increment during the exercise was similar (23.3 +/- 3.3 micromol/l/min on carvedilol and 20.0 +/- 3.6 micromol/l/min on placebo). During recovery, the mean rate of potassium decrement was 5.0 +/- 3.0 micromol/l/min and 6.7 +/- 2.7 micromol/l/min, respectively. Serum sodium, ionizedcalcium, insulin and plasma renin activity were similar before the exercise tests and did not change during the exercise. CONCLUSION:Carvedilol does not enhance the hyperkalemic effect of moderate physical exercise in anuric hemodialysis patients.