Heparin is a commonly used anticoagulant medication that helps prevent blood clots in patients undergoing surgery, dialysis, or receiving treatment for certain medical conditions. While heparin is generally considered safe, it can cause a potentially life-threatening side effect: hyperkalemia.

Heparin is a cornerstone of modern anticoagulation therapy, used extensively for the prevention and treatment of venous thromboembolism, as well as in the management of acute coronary syndromes. Common adverse effects include bleeding, osteoporosis with long-term use, and heparin-induced thrombocytopenia. However, electrolyte disturbances, specifically hyperkalemia, represent a less frequently discussed but potentially life-threatening complication.

Aldosterone acts on the distal tubules and collecting ducts of the nephron to promote sodium reabsorption and potassium excretion. In the setting of heparin-induced hypoaldosteronism, the kidneys lose their capacity to effectively excrete potassium. This results in a gradual accumulation of serum potassium, leading to hyperkalemia. The effect is often termed "selective hypoaldosteronism" because the glucocorticoid axis (cortisol production) remains intact.

In addition to direct enzymatic inhibition, heparin has been shown to decrease the number and affinity of angiotensin II receptors on zona glomerulosa cells. Angiotensin II is a primary stimulant for aldosterone secretion. By downregulating these receptors, heparin renders the adrenal gland less responsive to physiological stimuli that would normally trigger aldosterone release in response to hyperkalemia or hypovolemia.

Acute kidney injury, adrenal insufficiency, pseudohyperkalemia (hemolysis, thrombocytosis), medications (list above).

Not all patients develop hyperkalemia. Risk is highest with: