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Background: Resistant hypertension is a common clinical problem and greatly increases the risk of target organ damage. Methods: We evaluated the characteristics of 279 consecutive patients with resistant hypertension (uncontrolled despite the use of 3 antihypertensive agents) and 53 control subjects (with normotension or hypertension controlled by using Յ2 antihypertensive medications). Participants were prospectively examined for plasma aldosterone concentration, plasma renin activity, aldosterone to renin ratio, brain-type natriuretic peptide, atrial natriuretic peptide, and 24-hour urinary aldosterone (UAldo), cortisol, sodium, and potassium values while adhering to a routine diet. Results: Plasma aldosterone (P Ͻ.001), aldosterone to renin ratio (P Ͻ .001), 24-hour UAldo (P = .02), braintype natriuretic peptide (P = .007), and atrial natriuretic peptide (P=.001) values were higher and plasma renin activity (P=.02) and serum potassium (P Ͻ.001) values were lower in patients with resistant hypertension vs controls. Of patients with resistant hypertension, men had

These data indicate that the ARR is valid as a screening test for PA in African American and white patients on stable antihypertensive treatments, but a high percentage of false-positive results precludes using it for accurate diagnosis of PA.

Abstract-Experimental data indicate that the cardiorenal effects of aldosterone excess are dependent on concomitant high dietary salt intake. Such an interaction of endogenous aldosterone and dietary salt has not been observed previously in humans. We assessed the hypothesis that excess aldosterone and high dietary sodium intake combine to worsen proteinuria in patients with resistant hypertension. Consecutive subjects with resistant hypertension (nϭ84) were prospectively evaluated by measurement of 24-hour urinary aldosterone (Ualdo), sodium, and protein (Uprot) excretion. Subjects were analyzed according to aldosterone status (high: Ualdo Ն12 g/24 hours; or normal: Ͻ12 g/24 hours) and dietary salt intake based on tertiles of urinary sodium. Key Words: hypertension Ⅲ aldosterone Ⅲ salt Ⅲ proteinuria Ⅲ kidney A ldosterone excess is being increasingly recognized as a common cause of hypertension, with recent reports indicating a prevalence of primary aldosteronism (PA) of 5% to 10% among general hypertensive patients. 1-5 Among patients with resistant hypertension, PA is even more common, with a prevalence of Ϸ20%. 6 Animal models indicate that aldosterone excess, in addition to increasing blood pressure (BP), contributes directly to target-organ (heart, brain, and kidney) deterioration by inducing inflammation and perivascular fibrosis. 7-9 These same studies have been consistent in demonstrating that the pressor, proinflammatory, and profibrotic effects of aldosterone are dependent on concomitant high dietary salt intake. That is, the deleterious effects of aldosterone are minimized or even prevented by low dietary salt ingestion. Whether such an interaction between aldosterone and dietary salt occurs in humans is unknown.Increases in intracapillary pressure, structural damage of the glomerular membrane, and impaired endothelial function likely contribute to the development of albuminuria and proteinuria in hypertensive patients. 10 Proteinuria is an early sign of nephropathy associated with progressive glomerulosclerosis, tubulointerstitial inflammation, and scarring, with progressive renal function loss in both diabetic and nondiabetic subjects. 11 Proteinuria is also independently associated with increases in cardiovascular risk. [12][13][14][15] The present study was designed to evaluate the effects of endogenous aldosterone and dietary salt, separately and in combination, on proteinuria in subjects with resistant hypertension. In enrolling subjects with resistant hypertension, we were purposefully selecting a cohort known to be at high risk for hyperaldosteronism. Methods SubjectsConsecutive subjects referred to the University of Alabama at Birmingham Hypertension Clinic for resistant hypertension were prospectively evaluated. The protocol was approved by the University of Alabama at Birmingham Institutional Review Board for Human Use, and all of the subjects provided written informed consent before study participation. Resistant hypertension was defined as uncontrolled hypertension (Ͼ140/90 mm Hg) determi...

In spite of similar office BP, ABPM levels were higher in resistant hypertensive patients with H-Aldo. These results suggest that high aldosterone levels impart increased cardiovascular risk not reflected by office BP measurements.