Aldo is back: recent advances and unresolved controversies in hyperaldosteronism

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Abstract
Hyperaldosteronism in its various forms is a recognized secondary cause of hypertension, yet the frequency of these disorders and the appropriate evaluation of suspected patients remain controversial. This review will summarize recent literature concerning the frequency of hyperaldosteronism in the hypertensive population, insight from uncommon forms of hyperaldosteronism, and new developments in the diagnosis and treatment of this condition. Several series report that around 10% of hypertensive patients have some form of hyperaldosteronism, but aldosterone-producing adenomas are rare. Diagnostic criteria for idiopathic hyperaldosteronism remain controversial, as is the wisdom of widespread screening. Patients with even mild hyperaldosteronism, however, which could be a continuum with low-renin hypertension, may respond exceptionally well to mineralocorticoid antagonism. Eplerenone, a new mineralocorticoid receptor antagonist without antiandrogen side effects, has been an effective antihypertensive in clinical trials and appears to be particularly suitable for low-renin hypertensives. Accumulating evidence suggests that aldosterone excess is cardiotoxic and nephrotoxic, suggesting that mineralocorticoid blockade has specific benefits beyond blood pressure reduction. For patients with severe, confirmed hyperaldosteronism, selective adrenal vein sampling is the only reliable method for determining the source of the aldosterone. Hyperaldosteronism, when defined with liberal criteria, could account for a substantial portion of hypertension. Few of these patients will harbor adrenal adenomas, but those with severe hypertension and hypokalemia often require adrenal vein sampling to direct surgery. With more precise diagnostic strategies, better treatments, and evolving evidence of pathological consequences of aldosterone excess, subtle disorders of aldosterone excess demand precise definition and specific treatment.