In primary hyperaldosteronism, how does the RAAS respond and what is the expected renin level?

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Multiple Choice

In primary hyperaldosteronism, how does the RAAS respond and what is the expected renin level?

Explanation:
Autonomous aldosterone production from the adrenal cortex drives sodium and water retention, causing volume expansion and hypertension. That increased volume feeds back to the kidneys to suppress renin release, so the renin-angiotensin-aldosterone system becomes suppressed overall. The expected renin level is low (suppressed). This distinguishes primary hyperaldosteronism from secondary forms, where the stimulus to renin is present and renin is high, driving a secondary rise in aldosterone.

Autonomous aldosterone production from the adrenal cortex drives sodium and water retention, causing volume expansion and hypertension. That increased volume feeds back to the kidneys to suppress renin release, so the renin-angiotensin-aldosterone system becomes suppressed overall. The expected renin level is low (suppressed). This distinguishes primary hyperaldosteronism from secondary forms, where the stimulus to renin is present and renin is high, driving a secondary rise in aldosterone.

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