Primary aldosteronism as an early model of cardiovascular-kidney-metabolic disease: clinical reappraisal and salt-related pathophysiological insights

Primary aldosteronism (PA) is considered the epitome of the sodium-retentive disease and, although traditionally considered a benign form of hypertension because of the undetectable renin levels, it has robustly been associated with excess left ventricular hypertrophy, left ventricle fibrosis, vascular remodelling, microalbuminuria, endothelial dysfunction, and with a high risk of stroke, myocardial infarction, heart failure, and atrial fibrillation. Given the primary role of sodium and of its tissue accumulation in the spectrum of the cardio-kidney-metabolic (CKM) syndrome, we evaluated the effect of salt loading in PA, as a reversible model of CKM disease featuring sodium-avidity and excess organ damage. We primarily hypothesized that salt loading can exacerbate glomerular hyperfiltration and induce myocardial oedema, with consequent functional alterations, in patients with PA.