Mechanism of enhanced transcellular potassium-secretion in man with chronic renal failure.

Previous studies from our laboratory demonstrated that net K secretion in human rectum was 2.5-fold higher in patients with chronic renal failure than in controls. The present study was performed to determine whether K secretion in human large intestine involves an active process and whether an active transport process accounts, at least in part, for the rise in net K secretion in patients with renal insufficiency. Studies were performed under conditions when net water and electrolyte transport approached zero, and the observed distribution of K and Na across the rectal mucosa was compared to expected equilibrium values. In control subjects an active transport of 27.6 +/- 2.6 mV was observed for K and 63 +/- 4.2 mV for Na. Similar values were demonstrated in patients with chronic renal failure. The results of these studies demonstrated that net secretion of K and absorption of Na are governed, at least in part, by active transport processes, and suggest that, since active K secretion is not impaired, the rise in net K secretion in patients with renal insufficiency is caused by active secretion as well as by passive driving forces.

Increased secretion of potassium in the rectum of humans with chronic renal failure.

Previous studies have shown that the intestinal excretion of potassium increases in patients with renal failure and serves to guard against severe potassium retention. It is not known, however, whether the rise in intestinal potassium excretion occurs because of an increase in intestinal potassium secretion or a reduction in potassium absorption. Therefore, studies were performed to evaluate the rate of potassium secretion in the human rectum of controls and subjects with renal insufficiency, using a dialysis bag technique. The results demonstrate that net potassium secretion was increased in subjects with renal failure (-5.2 +/- 0.9 microEq X min-1) compared with the control value of -2.0 +/- 0.4 microEq (P less than .05). This change in intestinal secretion of potassium was shown to be independent of the passive effects of plasma potassium. The rise in potassium secretion, however, correlated directly with an increase in transepithelial potential difference (lumen-negative). Although plasma aldosterone levels were higher in patients than in controls, the scatter of data precludes an assessment of the role of aldosterone in the mechanism of the rise in potassium secretion. These data suggest that augmented intestinal potassium excretion in patients with chronic renal insufficiency is caused by increased net potassium secretion in the large intestine, and highlight the role of the intestine in maintaining potassium balance.