aldosterone escape
Summary
Phenomenon in which chronic aldosterone excess (e.g., Conn syndrome) initially expands volume but is then 'escaped' by pressure natriuresis and ANP, preventing edema. Hypokalemia and metabolic alkalosis persist because they are not escaped.
Detail
In primary hyperaldosteronism, aldosterone drives ENaC-mediated Na reabsorption in the cortical collecting duct, expanding ECF volume and raising BP. After several days, increased renal perfusion pressure (pressure natriuresis) and ANP/BNP release downregulate proximal Na reabsorption, allowing Na excretion to match intake — so patients are hypertensive but not edematous. The escape applies only to sodium/water; aldosterone's effects on K+ and H+ secretion are not escaped, so patients remain hypokalemic with metabolic alkalosis. This contrasts with secondary hyperaldosteronism in heart failure/cirrhosis, where the kidney perceives ongoing hypovolemia, so no escape occurs and edema/ascites develop. High-yield distinction explains why Conn's patients have hypertension without edema.
Sources
- First Aid for USMLE Step 1 2024
- Costanzo Physiology
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