Hyperkalemia

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

Etiology

• Spurious (Table 21–6)

  • 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