Potassium homeostasis and clinical implications

Abstract

The clinical estimation of potassium balance generally depends on the level of serum potassium. Since the extracellular fluid contains only 2 percent of the total body potassium, it must be recognized that potassium deficits are usually large before significant hypokalemia occurs, whereas smaller surfeits of potassium will cause hyperkalemia. The total body potassium is regulated by the kidney in which distal nephron secretion of potassium into the urine is enhanced by aldosterone, alkalosis, adaptation to a high potassium diet, and delivery of increased sodium and tubular fluid to the distal tubule. However, the distribution of potassium between the intracellular and extracellular fluids can markedly affect the serum potassium level without a change in total body potassium. Cellular uptake of potassium is regulated by insulin, acid-base status, aldosterone, and adrenergic activity. Hypokalemia, therefore, may be caused by redistribution of potassium into cells due to factors that increase cellular potassium uptake, in addition to total body depletion of potassium due to renal, gastrointestinal, or sweat losses. Similarly hyperkalemia may be caused by redistribution of potassium from the intracellular to the extracellular fluid due to factors that impair cellular uptake of potassium, in addition to retention of potassium due to decreased renal excretion. An understanding of the drugs that affect potassium homeostasis, either by altering the renal excretion of potassium or by modifying its distribution, is essential to the proper assessment of many clinical potassium abnormalities. Both hypokalemia and hyperkalemia may cause asymptomatic electrocardiographic changes, serious arrhythmias, muscle weakness, and death. Hypokalemia has also been associated with several other consequences, including postural hypotension, potentiation of digitalis toxicity, confusional states, glucose intolerance, polyuria, metabolic alkalosis, sodium retention, rhabdomyolysis, intestinal ileus, and decreased gastric motility and acid secretion.