The effects of captopril on serum digoxin and urinary urea and digoxin clearances in patients with congestive heart failure

Abstract

The effect of captopril as long-term treatment in 20 patients with congestive heart failure has been studied in a double-blind trial. Captopril caused a significant increase in serum digoxin levels. No patients developed evidence of digoxin toxicity. Serum and total body potassium rose and the frequency of ventricular arrhythmias showed a modest decline. Creatinine clearance and radioisotopically measured glomerular filtration rate fell, but there was a poor relationship between these and the increase in serum digoxin. In a further open study on 12 patients, creatinine, urea, and digoxin clearance were significantly reduced by captopril. However, digoxin clearance declined more than creatinine clearance (89 +/- 25 mumol/L to 69 +/- 22 mumol/L and 81 +/- 14 mumol/L to 72 +/- 19 mumol/L, respectively, p less than 0.05 for the difference). Fractional excretion of urea and digoxin filtered at the glomerulus declined, indicating greater tubular reabsorption or reduced tubular secretion of these compounds. Captopril causes an increase in serum digoxin by reducing renal clearance of the drug.