**1. Introduction**

Primary aldosteronism (PA) is the most common potentially curable form of hypertension with a prevalence of 5–10% in patients with hypertension [1–3] and is characterized by the excessive production of aldosterone. Aldosterone excess has detrimental effects independent of blood pressure control as demonstrated by the increased risk of cardiovascular and cerebrovascular events and target organ damage in patients with PA relative to matched patients with essential hypertension. PA is mainly caused by either an aldosterone-producing adenoma (APA) or bilateral adrenal hyperplasia (BAH). The diagnosis of an APA is appealing because hypertension can be cured or markedly improved by unilateral adrenalectomy and resolve the aldosterone excess in the majority of cases [4]. In contrast, patients with BAH are usually treated with a mineralocorticoid receptor antagonist but plasma renin levels should be monitored as a therapeutic response (as well as blood pressure) because suppressed renin, independent of blood pressure control, is associated with an increased risk of cardiometabolic events and death relative to patients with essential hypertension [5]. A landmark in PA research was

the discovery of germline and somatic mutations that drive the aldosterone overproduction in patients with PA, discoveries that were made possible by the application of next-generation sequencing [6–12]. The genetic basis of four familial forms of PA has now been described as well as somatic mutations in APAs and these are discussed in more detail below.

Herein, we outline novel contributions and major discoveries that have been made in the field of PA research over the last few years. We describe the genetic basis of familial forms of hyperaldosteronism and the identification of somatic mutations that lead to excess aldosterone production. Differential gene expression profiles between APAs and reference tissues are highlighted, as well as key signalling pathways and molecular mechanisms that may drive cell proliferation and constitutive aldosterone production in APAs. Additionally, the possible influence of genetics and genomics on surgical outcome and the potential application of next-generation sequencing methods and transcriptome profiling as possible prognostic tools are described.
