Is It the Beginning of the End for the Recumbent Saline Infusion Test?
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See related article, pp 989–994
In primary aldosteronism (PA), autonomous overproduction of the salt-retaining mineralocorticoid hormone, aldosterone, by the adrenal cortex leads to the suppression of its normal principal regulator, renin/angiotensin II.1 Aldosterone overproduction results in salt and water retention, causing hypertension and urinary K+ wasting, which eventually may lead to hypokalemia.1 Although once thought to account for <1% of hypertension, evidence accumulated during the past 2 to 3 decades suggests that the prevalence is much higher (5% to 10%) and most patients are normokalemic.2–4
Early diagnosis of PA is important because optimal hypertension control is often achieved only with either aldosterone receptor antagonists (spironolactone and eplerenone) or epithelial Na+ channel blockers (amiloride). Adrenal venous sampling selects those with aldosterone-producing adenoma from those with bilateral adrenal hyperplasia5 with the possibility of surgical cure. Furthermore, aldosterone excess has adverse effects in addition to those of hypertension alone–cardiac and vascular remodeling and fibrosis, heart attack, arrhythmias, stroke, and renal damage,6 making it imperative not to miss PA.
The US Endocrine Society guideline on detection, diagnosis, and management of PA has recommended that, instead of proceeding directly to subtype classification, patients who screen positive for PA by demonstrating elevated plasma aldosterone/renin ratio levels should undergo further testing to definitively confirm or exclude the diagnosis.7 This approach recognizes the possibility that elevated aldosterone/renin ratio values may represent false positives and permits identification of individuals who, by testing …