Aldosterone, Dietary Salt, and Renal Disease

Increased urinary albumin excretion (UAE) is an earlyindicator of glomerular damage and of increased cardiovas-cular risk. Systemic endothelial dysfunction, for which albuminuria is presumed to be a sensitive biomarker, likely underlies, at least in part, these combined cardiorenal effects.1 A large body of experimental data implicates the independent roles of aldosterone and high dietary salt ingestion in contributing to the development of kidney disease separate from the effects of high blood pressure.2,3 Less well documented is the degree to which aldosterone and dietary salt contribute to renal disease in humans and, in particular, how these factors interact to effect renal function. In this issue of Hypertension, Rossi et al4 report that patients with newly diagnosed hypertension who were con-firmed to have primary aldosteronism had greater UAE than newly diagnosed hypertensive patients without primary aldo-steronism. In all of the patients, urinary sodium excretion