Pathophysiology of potassium absorption and secretion by the human intestine

Gastroenterology. 1994 Aug;107(2):548-71. doi: 10.1016/0016-5085(94)90184-8.


When normal people ingest 90 mEq/day of K+ in their diet, they absorb about 90% of intake (81 mEq) and excrete an equivalent amount of K+ in the urine. Normal fecal K+ excretion averages about 9 mEq/day. The vast majority of intestinal K+ absorption occurs in the small intestine; the contribution of the normal colon to net K+ absorption and secretion is trivial. K+ is absorbed or secreted mainly by passive mechanisms; the rectum and perhaps the sigmoid colon have the capacity to actively secrete K+, but the quantitative and physiological significance of this active secretion is uncertain. Hyperaldosteronism increases fecal K+ excretion by about 3 mEq/day in people with otherwise normal intestinal tracts. Cation exchange resin by mouth can increase fecal K+ excretion to 40 mEq/day. The absorptive mechanisms of K+ are not disturbed by diarrhea per se, but fecal K+ losses are increased in diarrheal diseases by unabsorbed anions (which obligate K+), by electrochemical gradients secondary to active chloride secretion, and probably by secondary hyperaldosteronism. In diarrhea, total body K+ can be reduced by two mechanisms: loss of muscle mass because of malnutrition and reduced net absorption of K+; only the latter causes hypokalemia. Balance studies in patients with diarrhea are exceedingly rare, but available data emphasize an important role for dietary K+ intake, renal K+ excretion, and fecal K+ losses in determining whether or not a patient develops hypokalemia. The paradoxical negative K+ balance induced by ureterosigmoid anastomosis is described. The concept that fecal K+ excretion is markedly elevated in patients with uremia as an intestinal adaptation to prevent hyperkalemia is analyzed; we conclude that the data do not convincingly show the existence of a major intestinal adaptive response to chronic renal failure.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Adaptation, Physiological
  • Amiloride / pharmacology
  • Anastomosis, Surgical
  • Cation Exchange Resins / pharmacology
  • Colon / metabolism
  • Diarrhea / etiology
  • Diarrhea / metabolism
  • Feces / chemistry
  • Glucocorticoids / pharmacology
  • Humans
  • Hyperaldosteronism / complications
  • Hypokalemia / metabolism
  • Intestinal Absorption* / drug effects
  • Intestinal Mucosa / metabolism*
  • Intestine, Small / metabolism
  • Intestines / drug effects
  • Intestines / surgery
  • Ion Transport
  • Kidney Failure, Chronic / metabolism
  • Mineralocorticoids / pharmacology
  • Potassium / metabolism*
  • Potassium, Dietary / administration & dosage
  • Ureter / surgery
  • Urinary Diversion / adverse effects


  • Cation Exchange Resins
  • Glucocorticoids
  • Mineralocorticoids
  • Potassium, Dietary
  • Amiloride
  • Potassium