## Hyperkalemia Risk with ACE Inhibitors and ARBs **Key Point:** ACE inhibitors (and ARBs) reduce angiotensin II formation, which decreases aldosterone secretion, leading to reduced renal potassium excretion and hyperkalemia risk. ### Mechanism of Hyperkalemia 1. ACE inhibitors block angiotensin II production 2. Angiotensin II normally stimulates aldosterone release from the adrenal cortex 3. With reduced angiotensin II, aldosterone secretion falls 4. Aldosterone normally promotes Na^+^ reabsorption and K^+^ excretion in the collecting duct 5. Reduced aldosterone → decreased K^+^ excretion → hyperkalemia **High-Yield:** Hyperkalemia risk is especially high in patients with: - Chronic kidney disease (reduced GFR) - Diabetes mellitus - Concurrent use of potassium-sparing diuretics or NSAIDs - Baseline serum K^+^ > 5.0 mEq/L ### Monitoring and Management - Check baseline K^+^ and creatinine before initiating ACE inhibitor - Recheck K^+^ 1–2 weeks after initiation or dose increase - Educate patient to avoid potassium-rich foods and salt substitutes (KCl) - Consider dose reduction or discontinuation if K^+^ > 5.5 mEq/L **Warning:** Do NOT assume hyperkalemia is rare—it is a common cause of ACE inhibitor discontinuation in clinical practice, especially in India where CKD prevalence is high. ### Contrast with Other Agents | Drug Class | K^+^ Effect | Mechanism | | --- | --- | --- | | ACE inhibitors | ↑ (hyperkalemia risk) | ↓ Aldosterone | | ARBs | ↑ (hyperkalemia risk) | ↓ Aldosterone | | Thiazide diuretics | ↓ (hypokalemia) | ↑ K^+^ excretion | | Beta-blockers | ↑ (mild hyperkalemia) | ↓ Catecholamine-mediated K^+^ shift | | Calcium channel blockers | ↔ (no effect) | No RAS interaction | **Clinical Pearl:** In a patient on ACE inhibitor with hyperkalemia, first step is to check compliance with dietary potassium restriction and review concurrent medications (NSAIDs, K-sparing agents) before discontinuing the ACE inhibitor.
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