Renal function curve in patients with secondary forms of hypertension

Abstract

The causative mechanisms of hypertension were investigated by studying the renal function (pressure-natriuresis) curve in patients with primary aldosteronism (n = 6) and renovascular hypertension (n = 6). Before and after radical operation (removal of adenoma in primary aldosteron-ism and percutaneous transluminal angioplasty in renovascular hypertension), dietary NaCl intake was altered from 10 to 13 g/day in Week 1 to 1 to 3 g/day in Week 2. Mean arterial pressure (MAP) and urinary sodium excretion were measured on the last 3 days of each week. By restricting sodium intake before operation, MAP was reduced from 122 ± 7 to 113 ± 7 mm Hg (p < 0.025) in primary aldoste-ronism but not in renovascular hypertension (130 ± 6 to 128 ± 5 mm Hg). The renal function curve was drawn by plotting urinary sodium excretion on the ordinate and MAP on the abscissa before and after operation. The slope of the curve was analyzed between the plotted points, and each curve was extrapolated to zero sodium excretion as an estimate of the degree of shift of the curve along the MAP axis. Before, as compared with after operation, the extrapolated x-intercept of the curve was shifted rightward in both primary aldosteronism (111 ± 7 vs 87 ± 4 mm Hg; p < 0.025) and renovascular hypertension (128 ± 5 vs 95 ± 2 mm Hg; p < 0.025) and the slope was depressed in primary aldoste-ronism (16 ± 1 vs 40 ± 17 [mEq/day]7 mm Hg; p < 0.025) but not in renovascular hypertension (130 ± 75 vs 40 ± 13 [mEq/day]/mm Hg). After operation, the renal function curves in primary aldosteronism and renovascular hypertension were normalized. The rightward shift of the curve in renovascular hypertension probably was due to an increase in renal vascular resistance caused by the stenotic renal vascular lesion as well as to increased resistance caused by stimulation of the renin-angiotensin system. The rightward shift in primary aldosteronism presumably was due to enhance-ment of renal tubular sodium reabsorption by aldosterone; the depressed slope likely resulted from suppression of the renin-angiotensin feedback mechanism by the excess aldosterone and resultant volume expansion. Thus, an abnormal renal function curve seems to have played a major role in the genesis of each of these forms of secondary hypertension. © 1987 American Heart Association, Inc.