endocrine and metabolic disorders
Overview of Disorders of Potassium Concentration
Potassium metabolism
Dietary potassium intake normally varies between 40 and 150 mEq (40 and 150 mmol)/day. In the steady state, fecal losses are usually close to 10% of intake. The remaining 90% is excreted in the urine, so alternations in renal potassium secretion greatly affect potassium balance. When potassium intake is>150 mEq (> 150 mmol)/day, about 50% of the excess potassium appears in the urine over the next several hours. Most of the remainder is transferred into the intracellular compartment, thus minimizing the rise in serum potassium. When elevated potassium intake continues, aldosterone secretion is stimulated and thus renal potassium excretion rises. In addition, potassium absorption from stool appears to be under some regulation and may fall by 50% in chronic potassium excess. When potassium intake falls, intracellular potassium again serves to buffer wide swings in serum potassium concentration. Renal potassium conservation develops relatively slowly in response to decreases in dietary potassium and is far less efficient than the kidneys’ ability to conserve sodium. Thus, potassium depletion is a frequent clinical issue. Urinary potassium excretion of 10 mEq (10 mmol) /day represents near-maximal renal potassium conservation and implies significant potassium depletion. Potassium excretion can be either enhanced or diminished in acidosis depending upon the type of acidosis, volume status and renal function. Increased delivery of sodium to the distal nephrons, as occurs with high sodium intake or loop diuretic therapy, promotes potassium excretion. 