S-55-1: PRIMARY ALDOSTERONISM – WHERE TO FROM HER E?

Abstract

Over the past decade there have been remarkable advances in the pathophysiology of primary aldosteronism (PA); in contrast, there has been little if any change in the clinical management of PA for over 20 years. A patient suspected of PA is referred to an expert center, and their medications withdrawn for 4–6 weeks, with CCBs/alpha blockers used if needed to control blood pressure (BP).They undergo a single blood draw for plasma aldosterone concentration (PAC) and plasma renin activity or concentration (PRA/PRC), to establish the aldosterone to renin ratio (ARR). If the ARR 'suggests’ PA, the patient then undergoes confirmatory testing by one of at least five different procedures – to ensure no patient who does not have PA ever slips through the net. There are multiple reasons for change. First, in no country are more than 1% of hypertensives ever screened for PA. Secondly, a single blood draw for PAC is a very imperfect index of a patient’s actual aldosterone status; among those referred many are excluded on the basis of their PAC who in fact have PA. Third, the current work up – in addition to being exclusionary - is demanding and clunky. Fourth, the prevailing attitude among those treating hypertension is that if the BP is controlled all will be well, when in fact patients with PA have a three-fold higher risk profile than matched essential hypertensives with the same BP. What we are thus facing is a major public health crisis. There is finally increasing recognition that the current estimate of PA prevalence (5% - 10% of hypertensives) is far too low, and the actual prevalence in hypertensives is of the order of at least 30% (and of 10% in normotensives). The current protocols are useless facing figures such as these; what is needed are much simpler and inclusive measures to diagnose probable PA – rather than excluding all but the most obvious cases. This will require input not only from endocrinologists, but also from hypertension specialists, internists, primary care and public health physicians. It is important to distinguish newly presenting and established hypertension. When a patient is newly diagnosed with an elevated BP eschew immediate antihypertensive(s) and order a PRA/PRC assay. If renin is not suppressed, onto antihypertensives. If the renin is suppressed coach the patient to provide a 24 h urine collection for Na, K, and urinary excretion of aldosterone (UEA). If the UEA is < 6 mcg/24 h the patient does not have PA; if the UEA is 6–12, the patient may have PA; if the UEA is > 12 the patient has PA. For these two latter categories order 25 mg/d spironolactone and review at four weeks. If BP falls by < 10mmHg onto antihypertensives; if BP falls by > 10 mmHg continue spironolactone. Established hypertension is rather simpler. Add spironolactone 25 mg/d to current medication and review at 4 weeks. If BP falls < 10mmHg, discontinue; if BP falls > 10mmHg order a UEA. If UEA and BP are moderately elevated continue spironolactone, as such patients very probably have bilateral hyperaldosteonism; if UEA and BP are high, refer to an expert center. What this is calling for is a radical reassessment of how physicians should address hypertensive patients. The rationale is to save them from the double jeopardy of hypertension and PA, and the attendant increased morbidity and premature mortality. The time is now.