Potassium-lowering effect of albuterol for hyperkalemia in renal failure

To study the effect of specific beta 2-adrenergic stimulation on potassium metabolism in renal failure, we intravenously administered albuterol (Salbutamol) sulfate, 0.5 mg, to 20 patients with chronic renal failure (glomerular filtration rate, less than 5 mL/min) receiving maintenance hemodialysis. Within 30 minutes after albuterol administration, serum potassium level dropped from 5.6 +/- 0.2 (+/- SEM) to 4.5 +/- 0.2 mEq/L (5.6 +/- 0.2 to 4.5 +/- 0.2 mmol/L). There were no changes in plasma aldosterone levels or arterial pH, but blood glucose and serum insulin levels increased. Albuterol, however, induced similar decreases in serum potassium levels in three diabetic patients while free C peptide levels remained undetectable or subnormal after administration of the drug. Albuterol sulfate alone (0.5 mg intravenously) was also used to treat 24 patients with acute or chronic renal failure and hyperkalemia. Their serum potassium levels dropped from 7 +/- 0.2 mEq/L (7 +/- 0.2 mmol/L) to 5.6 +/- 0.2 mEq/L (5.6 +/- 0.2 mmol/L), 5.6 +/- 0.2 mEq/L (5.6 +/- 0.2 mmol/L), 6 +/- 0.2 mEq/L (6 +/- 0.2 mmol/L), and 6.2 +/- 0.2 mEq/L (6.2 +/- 0.2 mmol/L) at 30, 60, 180, and 360 minutes after receiving albuterol, respectively, and this was accompanied by reversal of the electrocardiographic manifestations of hyperkalemia. Despite inducing transient tachycardia, albuterol was remarkably well tolerated and no serious side effects were observed. beta 2-adrenergic stimulation of intracellular potassium uptake by albuterol is a safe and effective alternative for the treatment of hyperkalemia in renal failure.