In recent years, a substantial prevalence of primary aldosteronism (PA) has been
demonstrated in both normotensive and mildly hypertensive cohorts. Consequently,
a classic presentation of the syndrome, i. e. moderate-to-severe
and resistant hypertension with concomitant hypokalemia, should be considered a
tip-of-the-iceberg phenotype of a wide PA spectrum. Its entire range encompasses
the non-classic clinical forms of mild hypertension and prehypertension but also
several biochemical presentations, including patients who meet PA screening and
confirmation test criteria, as well as those with either of them and those with
other parameters indicating mineralocorticoid excess. In the current review,
research insights on the pathogenetic background and clinical significance of
autonomous aldosterone secretion (AAS) are presented, which is defined as a
constellation of either: 1) normotension, normokalemia, a positive PA screening
(high aldosterone-to-renin ratio) and/or confirmation test, or 2)
hypertension, normokalemia and a positive PA screening but negative confirmation
test. For this purpose, a literature search of the PubMed database was
conducted. Advances in immunohistochemistry and genetic sequencing of isolated
adrenal cells are provided as probable morphologic basis of the wide range of
aldosterone secretion autonomy. Also, the role of corticotropin as an
aldosterone secretagogue is discussed. To date, clinical studies depict
consequences of subclinical PA phenotypes, such as increased mortality and risk
of developing hypertension, impaired arterial and kidney function, association
with metabolic syndrome and age, as well as osteoporosis.