Primary Hyperaldosteronism
Autonomous aldosterone secretion, independent of the renin-angiotensin system, that drives renal sodium retention and potassium/hydrogen loss, producing hypertension with a suppressed renin that is the biochemical signature the diagnostic test is built to detect.
First principles
Primary hyperaldosteronism is autonomous secretion, not appropriate activation
Normally, aldosterone rises when renin senses reduced renal perfusion, forming a tightly regulated axis. In primary hyperaldosteronism, an adrenal adenoma (Conn's syndrome) or bilateral adrenal hyperplasia secretes aldosterone independently of this trigger. Because aldosterone is high without renin driving it, and the resulting volume expansion further suppresses renin through normal negative feedback, the defining biochemical pattern is high aldosterone with low (suppressed) renin: the opposite of what appropriate, renin-driven aldosterone excess (secondary hyperaldosteronism) would show.
Educational content pending clinical review. Not medical advice.