cardio:diuretics:mra
Potassium-Sparing Diuretics
Potassium-sparing diuretics act at the collecting duct.
They reduce sodium reabsorption while preserving potassium.
These agents have weak diuretic effect but important clinical roles.
Used in:
- Resistant Hypertension
- Prevention of hypokalemia
Site of Action
Collecting Duct
Normal physiology:
- Aldosterone → ↑ ENaC expression
- ↑ Sodium reabsorption
- ↑ Potassium secretion
Potassium-sparing agents interfere with this process.
Two Major Subclasses
[[cardio:diuretics:potassium_sparing:mra|Mineralocorticoid Receptor Antagonists (MRAs)]]
Mechanism:
- Block aldosterone receptor
- ↓ ENaC expression
- ↓ Sodium reabsorption
- ↑ Potassium retention
- ↓ Myocardial fibrosis
Agents:
Clinical Importance:
- Mortality reduction in HFrEF
- Preferred 4th-line agent in resistant hypertension
- Treat primary hyperaldosteronism
Key Feature:
- Neurohormonal blockade — not just diuresis
[[cardio:diuretics:potassium_sparing:enac|ENaC Inhibitors]]
Mechanism:
- Directly block epithelial sodium channel (ENaC)
- Reduce sodium reabsorption
- Reduce potassium secretion
Agents:
Clinical Use:
- Prevent hypokalemia from:
No mortality benefit in heart failure.
Electrolyte Effects
All potassium-sparing diuretics:
- ↑ Potassium
- Mild natriuresis
Risk:
- Hyperkalemia
- Worsened by:
MRAs vs ENaC Inhibitors
MRAs:
- Block aldosterone receptor
- Reduce cardiac remodeling
- Reduce mortality in HFrEF
- Cause endocrine side effects (spironolactone)
ENaC Inhibitors:
- Pure potassium preservation
- No cardiac remodeling benefit
- Used primarily for electrolyte balance
Clinical Pearls
- Weak diuretics
- Strong neurohormonal agents (MRAs)
- Essential in HFrEF
- Spironolactone causes gynecomastia
- Monitor potassium closely
- Hyperkalemia risk increases with RAAS blockade
Related
cardio/diuretics/mra.txt · Last modified: by andrew2393cns