Hyperkalemia
Basics
Basics

Basics
Description
Description
Description
- An 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 involves tightly coordinated mechanisms:
- After ingestion, K enters the portal circulation, stimulating pancreatic insulin release, which promotes entry of K into cells.
- In the kidneys, K stimulates renin release from juxtaglomerular cells, activating the renin-angiotensin-aldosterone system (RAAS). Angiotensin II in the lungs stimulates aldosterone secretion from the adrenal zona glomerulosa. Aldosterone acts on the renal collecting ducts to enhance K excretion and sodium reabsorption.
- Four major causes
- Increased load: either endogenous from tissue breakdown (i.e., rhabdomyolysis or hemolysis) or exogenous (dietary or iatrogenic), usually in association with impaired renal function due to chronic kidney disease (CKD)
- Decreased excretion (most common): due to reduced glomerular filtration rate or impaired aldosterone secretion
- Cellular redistribution: shifts from intracellular space (majority of K is intracellular) to extracellular space (as in metabolic acidosis, tissue injury)
- Pseudohyperkalemia: artificial elevation of K due to hemolysis of blood sample, thrombocytosis, or leukocytosis
Geriatric Considerations
Increased risk for hyperkalemia because of decline in renin and aldosterone production with age, which impairs renal K excretion, especially in the setting of comorbid conditions
Epidemiology
Epidemiology
Epidemiology
Prevalence
Prevalence
Prevalence
- 5–9% of hospitalized patients (1)
- 1–2% in general population but as high as 34% in patients with CKD
Etiology and Pathophysiology
Etiology and Pathophysiology
Etiology and Pathophysiology
- Impaired K excretion (most common)
- Renal insufficiency/failure, obstructive uropathy
- Addison disease
- Mineralocorticoid deficiency
- Type IV renal tubular acidosis
- Cirrhosis
- Congestive heart failure
- Sickle cell disease
- Amyloidosis
- Systemic lupus erythematosus
- Increased K intake (2)
- Bananas, potatoes, melons, citrus juice, avocados, red meat, nuts, and dried fruits
- Salt substitutes given to CKD patients
- Transcellular shift (redistribution)
- Metabolic acidosis
- Insulin deficiency
- Hyperglycemia (diabetic ketoacidosis or hyperosmolar hyperglycemic state)
- Tissue damage (rhabdomyolysis, tumor lysis syndrome, burns, trauma)
- Medication-induced (3)
- RAAS inhibitors
- K-sparing diuretics
- NSAIDs
- Heparin
- Trimethoprim
- β-Blockers
- Pseudohyperkalemia
- Hemolysis of blood sample (artifactual)
- Thrombolysis, thrombocytosis, leukocytosis
- Hereditary spherocytosis
- Infectious mononucleosis
- Familial pseudohyperkalemia
Genetics
Genetics
Genetics
Associated with some inherited diseases and conditions
- Familial hyperkalemic periodic paralysis
- Congenital adrenal hyperplasia
- Gordon syndrome
Risk Factors
Risk Factors
Risk Factors
- Impaired renal excretion of K
- Acidemia
- Massive cell breakdown (rhabdomyolysis, burns, trauma)
- Use of K-sparing diuretics
- Excess K supplementation
- Comorbid conditions: CKD, diabetes, heart failure, liver disease
General Prevention
General Prevention
General Prevention
Low K diet and oral supplement compliance in those at risk
Commonly Associated Conditions
Commonly Associated Conditions
Commonly Associated Conditions
- Acute kidney injury (AKI) or CKD, typically with GFR <30 mL/min
- Congestive heart failure; myocardial infarction
- Rhabdomyolysis
- Liver disease
- Use of offending medications
There's more to see -- the rest of this topic is available only to subscribers.
© 2000–2026 Unbound Medicine, Inc. All rights reserved
All content is protected by copyright and may not be used for AI model training or other unauthorized purposes.