The role of the large intestine in K+ excretion in chronic renal insufficiency was studied with a rectal dialysis technique in 14 normal subjects and eight normokalaemic, normotensive patients with chronic renal insufficiency. At initial intraluminal K+ concentrations of 10, 20, 30 and 45 mmol/l, net K+ secretion in patients with renal insufficiency was significantly greater than in normal subjects by approximately 1.8 mumol h-1 cm-2. The increase in net K+ secretion was more marked in those patients with creatinine clearances of less than 10 ml/min. In contrast, there were no significant differences in net Na+ and water transport, transmucosal potential difference and plasma aldosterone concentrations between the two groups. With an initial intraluminal K+ concentration of 30 mmol/l, the addition of amiloride (final concentration 1 mmol/l) to the rectal lumen decreased net Na+ absorption and transmucosal potential difference in normal subjects by 69% (P less than 0.005) and 31% (P less than 0.005) respectively, and in patients with renal insufficiency by 75% (P less than 0.05) and 36% (P less than 0.05) respectively, but there was no change in net K+ secretion in either group. These results indicate that the K+ secretory capacity of the rectal mucosa increases in chronic renal insufficiency, and the large intestine may therefore contribute to the maintenance of K+ homoeostasis as renal K+ excretion declines. Increased rectal K+ secretion in renal insufficiency occurs independently of changes in plasma K+ and aldosterone concentrations, net Na+ absorption and transmucosal potential difference, and may reflect stimulation of an active K+ secretory process.