**Elke Tatjana Aristizabal Prada 1, Isabella Castellano 2, Eva Sušnik 1, Yuhong Yang 1, Lucie S. Meyer 1, Martina Tetti 3, Felix Beuschlein 1,4, Martin Reincke <sup>1</sup> and Tracy A. Williams 1,3,\***


Received: 15 February 2018; Accepted: 6 April 2018; Published: 9 April 2018

**Abstract:** Primary aldosteronism is the most common form of endocrine hypertension with a prevalence of 6% in the general population with hypertension. The genetic basis of the four familial forms of primary aldosteronism (familial hyperaldosteronism FH types I–IV) and the majority of sporadic unilateral aldosterone-producing adenomas has now been resolved. Familial forms of hyperaldosteronism are, however, rare. The sporadic forms of the disease prevail and these are usually caused by either a unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia. Aldosterone-producing adenomas frequently carry a causative somatic mutation in either of a number of genes with the *KCNJ5* gene, encoding an inwardly rectifying potassium channel, a recurrent target harboring mutations at a prevalence of more than 40% worldwide. Other than genetic variations, gene expression profiling of aldosterone-producing adenomas has shed light on the genes and intracellular signalling pathways that may play a role in the pathogenesis and pathophysiology of these tumors.

**Keywords:** primary aldosteronism; aldosterone; aldosterone-producing adenoma; transcriptome profiing
