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For further information, see CMDT Part 21-05: Hyperkalemia

Key Features

Essentials of Diagnosis

  • Serum potassium > 5.0 mEq/L (> 5.0 mmol/L)

  • Hyperkalemia may develop in patients taking angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), and potassium-sparing diuretics, or their combination, even with no or only mild kidney dysfunction

  • The ECG may be normal despite life-threatening hyperkalemia

  • Measurement of plasma potassium level differentiates potassium leak from blood cells from elevated serum potassium

  • Rule out extracellular potassium shift from the cells in acidosis and assess renal potassium excretion

General Considerations

  • In acidosis, serum potassium concentration rises about 0.7 mEq/L for every decrease of 0.1 pH unit

  • In the absence of acidosis

    • Serum potassium concentration rises about 1 mEq/L when there is a total body potassium excess of 1–4 mEq/kg

    • However, the higher the serum potassium concentration, the smaller the excess necessary to raise the potassium levels further

  • Mineralocorticoid deficiency from Addison disease or chronic kidney disease (CKD) is another cause of hyperkalemia with decreased renal excretion of potassium

  • Mineralocorticoid resistance due to genetic disorders, interstitial kidney disease, or urinary tract obstruction also leads to hyperkalemia

  • The concomitant use ACE inhibitors and ARBs with spironolactone, triamterene, eplerenone, or β-blockers further increases the risk of hyperkalemia

  • Thiazide or loop diuretics and sodium bicarbonate may minimize hyperkalemia

  • Mild hyperkalemia that occurs in the absence of potassium-sparing drug therapy is usually due to type IV renal tubular acidosis

  • Hyperkalemia occurs commonly in AIDS

    • Impaired renal excretion of potassium can be due to use of pentamidine or trimethoprim-sulfamethoxazole or to hyporeninemic hypoaldosteronism


  • Spurious (Table 21–4)

    • Leakage from erythrocytes, marked thrombocytosis or leukocytosis

    • Repeated fist clenching during phlebotomy

    • Specimen from arm with K+ infusion

  • Decreased excretion

    • Kidney disease, acute and chronic

    • Renal secretory defects, eg, interstitial nephritis, sickle cell disease

    • Hyporeninemic hypoaldosteronism (type IV renal tubular acidosis), eg, diabetic nephropathy, heparin, AIDS; adrenal insufficiency

    • Drugs that inhibit K+ excretion (spironolactone, triamterene, eplerenone, ACE inhibitors, trimethoprim, nonsteroidal anti-inflammatory drugs)

  • Potassium shift from within the cell

    • Burns, rhabdomyolysis, hemolysis, severe infection, internal bleeding, vigorous exercise

    • Metabolic acidosis

    • Hypertonicity (solvent drag)

    • Insulin deficiency

    • Hyperkalemic periodic paralysis

    • Drugs: digitalis toxicity, β-adrenergic antagonists, succinylcholine, arginine

  • Excessive intake of K+

    • Ingestion or iatrogenic

Table 21–4.Causes of hyperkalemia.

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