Pathophysiology of potassium absorption and secretion by the human intestine.
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.
Agarwal
R
R
Department of Internal Medicine, Baylor University Medical Center, Dallas, Texas.
Afzalpurkar
R
R
Fordtran
J S
JS
D000222:Adaptation, Physiological; D000584:Amiloride / Q000494:pharmacology; D000714:Anastomosis, Surgical; D002411:Cation Exchange Resins / Q000494:pharmacology; D003106:Colon / Q000378:metabolism; D003967:Diarrhea / Q000209:etiology / Q000378:metabolism; D005243:Feces / Q000737:chemistry; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications; D007008:Hypokalemia / Q000378:metabolism; D007408:Intestinal Absorption / Q000187:drug effects; D007413:Intestinal Mucosa / Q000378:metabolism*; D007421:Intestine, Small / Q000378:metabolism; D007422:Intestines / Q000187:drug effects / Q000601:surgery; D017136:Ion Transport; D007676:Kidney Failure, Chronic / Q000378:metabolism; D008901:Mineralocorticoids / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D017419:Potassium, Dietary / Q000008:administration & dosage; D014513:Ureter / Q000601:surgery; D014547:Urinary Diversion / Q000009:adverse effects
D002411:Cation Exchange Resins; D005938:Glucocorticoids; D008901:Mineralocorticoids; D017419:Potassium, Dietary; D000584:Amiloride; D011188:Potassium