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ESSENTIALS OF DIAGNOSIS

  • 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.

GENERAL CONSIDERATIONS

Hypokalemia can result from insufficient dietary potassium intake, intracellular shifting of potassium from the extracellular space, or potassium loss (renal or extra-renal) (Table 21–3). Genetic disorders can be associated with some electrolyte disturbances (eTable 21–1). A low dietary potassium intake is usually not sufficient as the kidneys can lower urine potassium excretion to very low levels (less than 15 mEq/L). Shift of potassium into cells is increased by 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 such that hypokalemia is often refractory to treatment until the magnesium deficiency is corrected. Loop diuretics (eg, furosemide) cause substantial renal potassium and magnesium losses.

Table 21–3.Causes of hypokalemia.
eTable 21–1.Genetic disorders associated with electrolyte metabolism disturbances.

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