What is the most common cause of secondary hyperaldosteronism?

The most common cause of secondary hyperaldosteronism is renal artery stenosis. In this condition, the narrowing of the renal artery leads to decreased blood flow to the affected kidney. As a result, the kidney perceives a state of low perfusion or reduced blood volume, which stimulates the juxtaglomerular cells to increase production of renin. Elevated renin then catalyzes the conversion of angiotensinogen to angiotensin I, which is subsequently converted to angiotensin II. Angiotensin II promotes the secretion of aldosterone from the adrenal cortex, leading to increased sodium and water retention, contributing to the development of hypertension and fluid overload.

Although conditions like congestive heart failure and hypovolemia can also cause secondary hyperaldosteronism, they typically do so in specific contexts. Congestive heart failure can lead to reduced cardiac output and perceived hypovolemia, stimulating renin-angiotensin-aldosterone system (RAAS) activation. Hypovolemia directly shrinks effective circulating volume, triggering similar hormonal responses. However, renal artery stenosis remains the most common and a clear-cut identifiable cause of secondary hyperaldosteronism, manifesting primarily through its direct effects on renal blood