Primary Aldosteronism.

Abstract

In 1955 Dr Jerome Conn first documented primary aldosteronism (PA). Since then, screening, diagnosis and treatment have developed, in the process both refining and complicating management. Currently, screening requires 4-6 weeks of lead-up, including major changes in antihypertensive therapy, followed by a blood draw for plasma aldosterone concentration (PAC) and plasma renin activity (PRA) or concentration (PRC). Screening is considered indicative of PA on the basis of the PAC and the aldosterone to renin ratio (ARR). This is then followed by one or more of 6 confirmatory/exclusion tests. Three things have changed. First is now incontrovertible evidence that a single spot PAC is a deeply flawed index of true aldosterone status, so that many referred patients with PA fall at the first hurdle. A valid index of aldosterone status is an integrated value, measured as urinary aldosterone excretion (UEA) over 24 hours. On the basis of the UEA, the prevalence of PA appears to be 3-5 times higher than the currently accepted figure of 5-10% of hypertensives. The second is the recognition that inadequately treated PA has a cardiovascular risk profile ∼threefold that of matched essential hypertensives. Third is the realization that <1% of hypertensives are ever screened for PA, who are thus in double jeopardy for the risks of untreated PA on top of those for hypertension per se. Taken together, this a major if occult public health issue; if it is to be addressed, radical changes in management are needed. Some are in screening, which needs to be simply done on all newly-presenting hypertensives; others are major simplifications of screening in established hypertension. The front-line actors need to be Internists/Primary Care Providers; the costs will be significant, but much less than those of increased morbidity/premature mortality in unrecognised PA. Possible suggestions as to how best to address this constitute the final chapter of this article.