• Hyperkalemia is a common electrolyte disorder defined as a plasma potassium (K) concentration >5.5 mEq/L (>5 mmol/L).
  • Hyperkalemia depresses cardiac conduction and can lead to fatal arrhythmias.
  • Normal K regulation
    • Ingested K enters portal circulation; pancreas releases insulin in response. Insulin facilitates K entry into cells.
    • K in renal circulation causes renin release from juxtaglomerular cells, leading to activation of angiotensin I, which is converted to angiotensin II in lungs. Angiotensin II acts in adrenal zona glomerulosa to stimulate aldosterone secretion. Aldosterone, at the renal collecting ducts, causes K to be excreted and sodium to be retained.
  • Four major causes
    • Increased load: either endogenous from tissue release or exogenous from a high intake, usually in association with decreased excretion
    • Decreased excretion: due to decreased glomerular filtration rate or impaired aldosterone secretion
    • Cellular redistribution: shifts from intracellular space (majority of K is intracellular) to extracellular space
    • Pseudohyperkalemia: related to red cell lysis during collection or transport of blood sample, thrombocytosis, or leukocytosis

Geriatric Considerations
Increased risk for hyperkalemia because of decreases in renin and aldosterone as well as comorbid conditions


Incidence is higher in patients of older age, male sex, worse kidney function, comorbidities, and use of renin angiotensin-aldosterone system inhibitors (1).


  • 1–10% of hospitalized patients
  • 2–3% in general population but as high as 50% in patients with chronic kidney disease (2)

Etiology and Pathophysiology

  • Pseudohyperkalemia
    • Hemolysis of red cells in phlebotomy tube (spurious result is most common)
    • Thrombolysis
    • Leukocytosis (reverse pseudohyperkalemia)
    • Thrombocytosis
    • Hereditary spherocytosis
    • Infectious mononucleosis
    • Traumatic venipuncture or fist clenching during phlebotomy (spurious result)
    • Familial pseudohyperkalemia
  • Increased K intake (3)
    • Banana, potatoes, melons, citrus juice, and avocados
    • Salt substitutes given to chronic kidney patients
    • Clay ingestion
    • Consuming burn match heads
  • Transcellular shift (redistribution)
    • Metabolic acidosis
    • Insulin deficiency
    • Hyperglycemia (diabetic ketoacidosis or hyperosmolar hyperglycemic state)
    • Tissue damage (rhabdomyolysis, burns, trauma)
    • Cocaine abuse
    • Exercise with heavy sweating
  • Impaired K excretion
    • Renal insufficiency/failure
    • Addison disease
    • Mineralocorticoid deficiency
    • Primary hyporeninemia, primary hypoaldosteronism
    • Type IV renal tubular acidosis (hyporeninemic hypoaldosteronism)
    • Obstructive uropathy
    • Cirrhosis
    • Congestive heart failure
    • Sickle cell disease
    • Amyloidosis
    • Gordon syndrome
    • Systemic lupus erythematosus
  • Medication-induced (numerous)

Associated with some inherited diseases and conditions

  • Familial hyperkalemic periodic paralysis
  • Congenital adrenal hyperplasia

Risk Factors

  • Impaired renal excretion of K
  • Acidemia
  • Massive cell breakdown (rhabdomyolysis, burns, trauma)
  • Use of K-sparing diuretics
  • Excess K supplementation
  • Comorbid conditions: chronic kidney disease, diabetes, heart failure, liver disease

General Prevention

Low K diet and oral supplement compliance in those at risk

Commonly Associated Conditions

  • Chronic kidney disease
  • End-stage renal disease
  • Congestive heart failure
  • Myocardial infarction
  • Rhabdomyolysis
  • Liver disease
  • Use of medications such as ACE inhibitors or angiotensin II receptor blockers

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