Extract

Mansoor et al report eight subjects with presumed primary aldosteronism presenting as “hypertensive emergencies.”1 This retelling of an old observation is worthy of recognition, as many individuals erroneously believe primary aldosteronism to be a mild and relatively innocuous form of hypertension. In the past 50 years the diagnosis of primary aldosteronism has moved from a 2-week, metabolic ward exercise offered by a small number of institutions with the requisite techniques for measuring aldosterone and renin under very exacting clinical conditions of sodium loading and sodium and volume depletion to a simpler outpatient screening test (plasma aldosterone [PA]–to-renin [PRA] ratios) followed by more specific diagnostic and localizing tests.2 Several caveats are appropriate regarding the use of this ratio. False positive results (ie, ratios greater than 20 or 30) can be obtained frequently by the use of a denominator (PRA) that is below the typical limit of sensitivity (ie, 0.1 to 0.7). Setting the lowest value for PRA at 0.7 then requires that PA be ≥14. The patient designated as case 5 in the Mansoor et al report had PA/PRA of 150 and 250 because of the use of 0.1 for PRA.1

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