OACE inhibition does not interfere with acute extrarenal or renal potassium disposal in chronic renal failure

The influence of angiotensin converting enzyme (ACE) inhibition on acute extrarenal and renal potassium elimination in stable chronic renal failure has been examined in 10 male patients median age 44 y; mean CLCR 42 ml.min-1.1.73 m-2. In a double blind, placebo-controlled cross-over study, K+ 0.3 or 0.4 mmol.kg-1 body weight was infused IV on two occasions while the patients also received an infusion either of placebo or 0.5 mg of the ACE inhibitor perindoprilat in random order. Plasma K+ levels and urinary K+ excretion were measured at regular intervals. During the study patients adhered to an isocaloric diet providing a standardised daily intake of potassium and sodium (50 mmol K+ and 40 mmol Na+). The median rise in plasma K+ was not significantly different after placebo (delta K 0.66 mmol.l-1) compared with to the infusion of perindoprilat (delta K 0.66 mmol.l-1). The median baseline urinary K+ excretion rate was 6.5 mmol.3 h-1 before the placebo infusion and 5.9 mmol.3 h-1 before infusion of perindoprilat. During the potassium load, the urinary excretion rate rose to 16.1 mmol.3 h-1 (after placebo) and 15.1 mmol.3 h-1 after perindoprilat in the first 3 h, and it returned almost to the baseline value within the next 3 h (5.6 mmol.3 h-1 after placebo and 5.7 mmol.3 h-1 after perindoprilat); the differences were not statistically significant. With perindoprilat a decrease in mean arterial blood pressure and ACE activity, an increase in renin plasma activity and a decrease in aldosterone concentrations were observed compared to the placebo infusion. There was no significant differences plasma in adrenaline or insulin levels after either infusion. Thus, ACE inhibition did not interfere either with the extrarenal or the renal disposal of an acute potassium load in patients with chronic renal failure.