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(Hypertension. 2006;48:209.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

Aldosterone, Dietary Salt, and Renal Disease

Eduardo Pimenta; David A. Calhoun

From the Department of Vascular Biology and Hypertension, University of Alabama at Birmingham.

Correspondence to Eduardo Pimenta, Department of Vascular Biology and Hypertension, University of Alabama at Birmingham, 933 19th St South, Room 115, Birmingham, AL 35294. E-mail eduardo.pimenta@ccc.uab.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Increased urinary albumin excretion (UAE) is an early indicator of glomerular damage and of increased cardiovascular 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 confirmed to have primary aldosteronism had greater UAE than newly diagnosed hypertensive patients without primary aldosteronism. In all of the patients, urinary sodium excretion independently predicted UAE. These results both compare and contrast with recent results from Framingham investigators who found that in a cohort of normotensive and hypertensive subjects, UAE was positively associated in a continuous fashion with urinary sodium excretion.⁵ No such association was seen with serum aldosterone, although UAE was higher in subjects in the highest quintile of serum aldosterone levels. These 2 studies emphasize the importance of the combined roles of aldosterone and dietary salt ingestion in the progression of kidney disease while also generating important research questions to further explore the clinical ramifications of this interaction.

A large number of animal studies have confirmed the . . . [Full Text of this Article]

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