The first section (mutations) will address the (relatively) novel data on mutations causing hyperaldosteronism. The second section (mechanisms) will cover perhaps the least well-understood facet of PA, the genesis of the well-described heightened cardiovascular risk. The third section deals with clinical issues—prevalence, recognition, referrals, and the necessity to recognize PA as a major public health problem. The take home messages are 4-fold: that somatic mutations in the adrenal cortex account for most but not (yet?) all cases of unilateral PA and possibly bilateral PA; that familial PA reflects a variety of germline mutations, but is relatively rare; that how elevated aldosterone levels for sodium status causes increased cardiovascular risk remains unknown; and finally, that PA represents a major and hitherto unrecognized public health problem.
