Pathophysiology of potassium absorption and secretion by the human intestine

• Published in: Gastroenterology (New York, N.Y. 1943) Vol. 107; no. 2; p. 548
• Main Authors: Agarwal, R, Afzalpurkar, R, Fordtran, J S
• Format: Journal Article
• Language: English
• Published: United States 01-08-1994
• Subjects: 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
• ISSN: 0016-5085
• 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.