Potassium-aldosterone response in dogs with chronic renal insufficiency.

To evaluate the potassium-aldosterone axis in chronic renal insufficiency, the plasma concentration of aldosterone was measured before and after a 50-mEq potassium challenge in dogs with intact kidneys (glomerular filtration rate 52 +/- 3.1 ml/min) and in dogs with one remnant kidney (glomerular filtration rate 16.1 +/- 2.1 ml/min). Fasting concentrations of circulating potassium and aldosterone and urinary potassium excretion rates were similar in both groups. In the 5 h following potassium chloride administration, less of the potassium load was excreted by dogs with one remnant kidney (30.2 +/- 3.3%) than by normal dogs (55.6 +/- 7.3%; p less than 0.01); serum potassium rose significantly more in dogs with chronic renal insufficiency than in normal animals. After potassium chloride, plasma aldosterone increased in both groups, but the increments in dogs with one remnant kidney were twice the increases in normal dogs (p less than 0.01). The increases in plasma aldosterone per unit increment in serum potassium, however, were similar in both groups (14.5 vs. 13.8 ng X dl-1/mEq X l-1). Thus, the hyperkalemia that follows a potassium load in dogs with chronic renal insufficiency is not due to a failure to secrete aldosterone but to a decrease in potassium excretion in the setting of decreased renal mass.