## Most Common Cause of Hyperkalemia Among Diuretics **Key Point:** Potassium-sparing diuretics (aldosterone antagonists and epithelial Na⁺ channel blockers) are the most common diuretic class causing hyperkalemia, occurring in 5–10% of patients on chronic therapy. ### Mechanism of Hyperkalemia with K⁺-Sparing Diuretics 1. **Spironolactone** (aldosterone antagonist): - Blocks mineralocorticoid receptor in the collecting duct - Prevents aldosterone-mediated K⁺ secretion - Results in K⁺ retention and ↑ urinary Na⁺ excretion 2. **Amiloride & Triamterene** (ENaC blockers): - Directly inhibit epithelial Na⁺ channel in collecting duct - Reduce Na⁺ reabsorption → ↓ driving force for K⁺ secretion - K⁺ accumulates in tubular lumen and is reabsorbed ### Risk Factors for Hyperkalemia | Risk Factor | Mechanism | |-------------|----------| | **CKD (eGFR < 30)** | Reduced renal K⁺ excretion capacity | | **Diabetes mellitus** | Hyporenininemic hypoaldosteronism; impaired K⁺ secretion | | **Concurrent ACE-I/ARB** | Both reduce aldosterone → additive K⁺ retention | | **NSAIDs** | ↓ Renin release → ↓ aldosterone → K⁺ retention | | **Dehydration** | ↓ GFR → reduced K⁺ clearance | **High-Yield:** The combination of K⁺-sparing diuretics + ACE inhibitor/ARB + CKD is a **classic hyperkalemia triad** tested in NEET PG. ### Why Other Diuretics Do NOT Cause Hyperkalemia | Class | Effect on K⁺ | Reason | |-------|--------------|--------| | **Loop diuretics** | ↓↓ (hypokalemia) | Increase distal Na⁺ delivery + RAAS activation | | **Thiazides** | ↓ (hypokalemia) | Similar mechanism to loop diuretics, less potent | | **Osmotic diuretics** | ↓ (hypokalemia) | Osmotic effect → K⁺ wasting; no aldosterone effect | **Clinical Pearl:** Spironolactone is increasingly used in heart failure and resistant hypertension, making hyperkalemia a real clinical concern. Baseline K⁺ and renal function MUST be checked before initiation and monitored every 1–2 weeks in the first month. **Mnemonic: SHARP-K** — **S**pironolactone, **H**yperkalemia, **A**ldosterone antagonist, **R**etains K⁺, **P**otassium-sparing, **K**⁺ rises.
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