Quinapril administration in hemodynamically stable rats with reduced renal mass maintained serum potassium levels without causing severe hyperkalemia, even during high potassium intake.
Does quinapril cause severe hyperkalemia in hemodynamically stable subjects with reduced renal mass and renal dysfunction?
This preclinical study suggests that ACE inhibition does not inherently cause severe hyperkalemia in stable renal dysfunction, challenging widespread clinical assumptions.
Hyperkalemia is widely viewed as a common complication of ACE inhibition in azotemic patients. These renal failure patients are the patients who benefit most from ACE inhibition. Because we could not confirm this notion after a retrospective evaluation of 236 azotemic patients, we studied 2 models of renal mass reduction. In the first, we did a 5/6 nephrectomy (Nx) on rats and studied them 2 weeks after surgery (before chronic renal changes had developed). A second group was studied 16 weeks after Nx, once chronic renal failure was established. Rats in both models were treated with quinapril in drinking water. After baseline evaluation, we challenged them either by a high-K(+) diet or by blocking aldosterone receptors. We found that although quinapril blocked the K(+)-induced increase in aldosterone, serum K(+) levels and K(+) balance were maintained before and during high K(+) intake or during simultaneous spironolactone administration. We conclude that in hemodynamically stable rats with reduced renal mass and renal dysfunction, the administration of an ACE inhibitor does not cause severe hyperkalemia.
García et al. (Sat,) conducted a other in Renal failure and azotemia (n=236). Quinapril was evaluated on Serum potassium levels and potassium balance. Quinapril administration in hemodynamically stable rats with reduced renal mass maintained serum potassium levels without causing severe hyperkalemia, even during high potassium intake.