Primary Aldosteronism: Seismic Shifts
Abstract
Jerome Conn, the father of primary aldosteronism (PA), proposed that the syndrome may account for approximately 20% of patients with blood pressure (BP) elevation. For decades thereafter, conventional wisdom considered PA a rare (<1%) and relatively benign form of hypertension, which we now know is not the case. The first seismic shift came with the introduction of screening for PA by the aldosterone-to-renin ratio (ARR); on this basis, followed by confirmatory/exclusion testing, it is now recognized that PA represents 5–10% of hypertension. Over the past 5 years, there have been two more major advances. The first is the demonstration that a variety of somatic—ie, confined to the adrenal cortex—mutations have been found in what are now most aldosterone-producing adenomas. The first, and most common, mutation was that in KCNJ5, a component of the Kir3.4 potassium channel; subsequently, mutations in Na+ and Ca++ ATPases, Ca++ channels, and β-catenin have been described. The initial findings have been confirmed and replicated worldwide (1), ongoing exploration is intense, and the diagnostic and therapeutic aspects are yet to be determined.
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