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  • Serum potassium < 3.5 mEq/L (3.5 mmol/L).

  • Severe hypokalemia may induce arrhythmias and rhabdomyolysis.

  • Assessment of urine potassium excretion (urine potassium to creatinine ratio) can distinguish renal from nonrenal loss of potassium.


Hypokalemia can result from intracellular shifting of potassium from the extracellular space, potassium loss (renal or extrarenal) (Table 23–3), or rarely insufficient dietary potassium intake. Rare genetic disorders can be associated with electrolyte metabolism disturbances (eTable 23–1). A low dietary potassium intake is usually not sufficient to cause hypokalemia as the kidneys can lower urine potassium excretion to very low levels (less than 15 mEq/L) to adjust for dietary amounts. The shift of potassium into cells is increased by both insulin and beta-adrenergic stimulation. Excess potassium excretion by the kidneys is usually due to increased aldosterone action in the setting of preserved delivery of sodium to the distal nephron. Magnesium is an important regulator of potassium handling and low levels lead to persistent renal excretion of potassium; hypokalemia is often refractory to treatment until the magnesium deficiency is corrected. Several classes of diuretics, carbonic anhydrase inhibitors, loop diuretics and thiazide diuretics cause substantial renal potassium and magnesium losses.

eTable 23–1.Genetic disorders associated with electrolyte metabolism disturbances.
Table 23–3.Causes of hypokalemia.

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