secondary hyperaldosteronism

Secondary hyperaldosteronism results from physiologic stimulation of aldosterone secretion through the RAAS pathway, typically in response to decreased effective circulating volume or renal perfusion. The pathophysiology involves: (1) Reduced renal perfusion or effective blood volume triggers renin release from juxtaglomerular cells, (2) Renin converts angiotensinogen to angiotensin I, which is converted to angiotensin II by ACE, (3) Angiotensin II stimulates aldosterone synthesis in the zona glomerulosa. Major causes include renovascular disease (renal artery stenosis), congestive heart failure, cirrhosis with ascites, nephrotic syndrome, and diuretic use. Clinically, patients may present with hypertension, hypokalemia, and metabolic alkalosis, but the underlying condition often dominates the presentation. Laboratory findings show elevated aldosterone AND elevated renin (key distinction from primary hyperaldosteronism where renin is suppressed). The aldosterone-to-renin ratio is typically normal or low, unlike primary hyperaldosteronism where it's elevated. Treatment focuses on addressing the underlying cause and may include ACE inhibitors or ARBs to block the RAAS pathway.