Lisinopril causes hyperkalemia primarily by reducing aldosterone, which impairs renal potassium excretion.
ACE inhibitors like lisinopril block angiotensin II formation, leading to decreased aldosterone secretion.
Reduced aldosterone diminishes potassium secretion in the distal renal tubules.
Risk is significantly higher in patients with kidney disease, diabetes, or those taking potassium supplements/sparing diuretics.
Monitoring serum potassium and renal function is essential after initiation or dose changes.
Lisinopril, an ACE inhibitor, prevents the conversion of angiotensin I to angiotensin II. Angiotensin II normally stimulates the adrenal cortex to release aldosterone. Aldosterone acts on the distal convoluted tubule and collecting duct of the nephron to promote sodium reabsorption and potassium excretion into the urine. By lowering aldosterone levels, lisinopril reduces this excretory pathway, causing potassium retention. This effect is dose-dependent and exacerbated by impaired renal function (reduced GFR limits distal flow and potassium delivery), concurrent use of potassium-sparing diuretics (e.g., spironolactone), NSAIDs, or high dietary potassium intake. Clinically significant hyperkalemia (K+ > 5.5 mEq/L) can lead to fatal arrhythmias.
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