Recently, it has been suggested that primary aldosteronism (PA) is associated with a variety of cardiac, vascular, metabolic, and renal sequelae that reflect the capability of elevated aldosterone to induce organ damage beyond that induced by hypertension itself. The evidence supporting of these views has been obtained from experiments conducted in rodents and clinical studies conducted in patients with this endocrine disorder. It has been suggested that untoward effects of high-salt intake are dependent on activation of mineralocorticoid receptors that might result from increased oxidative stress and changes in the intracellular redox potential. Unilateral adrenalectomy or treatment with mineralocorticoid receptor antagonists are the current options for treating an aldosterone-producing adrenal adenoma or idiopathic adrenal hyperplasia. Treatments are largely effective in correcting hypertension and hypokalemia, and currently available information on their capability to prevent deterioration of renal function indicates that surgery and medical treatment are equally beneficial in the long term. This editorial review will focus on the renal aspects of PA and highlights the role of the kidney as a key determinant of both adaptation to aldosterone-induced volume retention and response of blood pressure to treatment.
