1. The renal and metabolic effects of the sulphamoylbenzoic acid diuretic,
piretanide, have been studied, under controlled dietary conditions, in 39 patients with congestive
cardiac failure. 2. In acute studies, peak saluresis occurred within 4 h of oral
piretanide administration; saluresis was complete within 6 h, after which a significant antidiuretic effect was observed. Addition of
triamterene, 50 mg, blunted the 0-6 h kaliuretic effect of
piretanide. Over 24 h,
piretanide, alone, caused insignificant urinary losses of
potassium when compared with control. 3. In comparative studies, the
piretanide dose-response curve was found to be parallel to that of
frusemide over the dose range studied. The 0-6 h saluretic responses of
piretanide, 6, 12 and 18 mg, were found to be equivalent to
frusemide, 40, 80 and 120 mg respectively. The collective mean ratios of all the saluretic responses to each dose of
piretanide with the corresponding dose of
frusemide was observed to be 0.99 +/- 0.12, over 0-6 h period, and 0.86 +/- 0.09 over the 24 h period. The relative potency of
piretanide, when compared with
frusemide was found to be 6.18 (95% confidence limits 4.87-8.33), over the 0-6 h period, and 4.73 (95% confidence limits 3.65-6.14), over 24 h period. 4. In 15 patients in severe
cardiac failure, urinary recovery of
piretanide, over first 6 h, at the start of treatment was 21.2 +/- 2.1% while efficiency of the diuretic (mmol Na/mg drug) was 47.3 +/- 4.1. Long-term
piretanide therapy was continued in the same group for up to and in some cases over 3 years. No other
diuretics or
potassium supplements were given.
Piretanide dosage ranged from 6 to 24 mg day-1 according to clinical need. Plasma
potassium fell significantly at 12 and 24 months, though remaining within the normal range. At these same times, significant elevations in both plasma
urate and total fasting
cholesterol were observed. Two patients developed overt
gout on high dose
piretanide therapy (24 mg day-1).
Piretanide was well tolerated, and effective in the management of congestive
cardiac failure without any other recognized metabolic or electrolyte changes.