American Board of Surgery Qualifying Exam (ABS QE) Practice Test

In primary hyperaldosteronism, the body experiences increased secretion of aldosterone from the adrenal glands, often due to an adrenal adenoma or hyperplasia. This excess aldosterone causes increased sodium retention, which leads to elevated blood volume and hypertension. As a consequence of the expanded blood volume and increased blood pressure, the body compensates by reducing the production of renin; this is a result of the negative feedback mechanism. The juxtaglomerular cells in the kidneys, which produce renin, sense the increase in blood volume and pressure, leading to suppression of renin secretion. Therefore, in primary hyperaldosteronism, it is typical to observe low renin levels, reflecting this compensatory response.

The reasoning for low renin levels helps delineate primary hyperaldosteronism from secondary causes of hyperaldosteronism, where renin levels would typically be elevated due to signaling from factors like renal artery stenosis or other conditions leading to reduced renal perfusion. Recognizing the characteristic finding of low renin in primary hyperaldosteronism is crucial for accurate diagnosis and management.