Abstract
There have been 2, and possibly 3, major questions for primary aldosteronism (PA)
answered at least in principle over the past 5 years. The first is that of
somatic mutations underlying the majority of aldosterone producing adenomas. The
second is the extension of our knowledge of the genetics of familial
hypertension, and the third the role of renal intercalated cells in sodium
homeostasis. New questions for the next 5 years include a single accepted
confirmatory/exclusion test; standardisation of assays and cut-offs;
alternatives to universal adrenal venous sampling; reclassification of ‘low
renin hypertension’; recognition of the extent of ‘occult’ PA; inclusion of
low-dose mineralocorticoid receptor antagonist in first-line therapy for
hypertension; and finally, possible resolution of the aldosterone/inappropriate
sodium status enigma at the heart of the cardiovascular damage in PA.
Key words
aldosterone - familial hyperaldosteronism type II and III - lateralisation - APA -
ACTH - endogenous ouabain - mineralocorticoid receptor antagonist
