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.