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July 1982

Renal Function and Hemodynamic Studies in Low- and Normal-Renin Essential Hypertension

Author Affiliations

From the Medical and Research Services, Harry S. Truman Memorial Veterans Hospital (Drs Bauer and Brooks and Ms Burch); and the Department of Medicine, University of Missouri Health Sciences Center (Drs Bauer and Brooks), Columbia.

Arch Intern Med. 1982;142(7):1317-1323. doi:10.1001/archinte.1982.00340200077018

• Reduced renal blood flow has been suggested to be both a cause and a consequence of essential hypertension. To test these hypotheses, techniques for the clearance of inulin (Cin) and p-aminohippurate (Cpah) were used to assess renal function and hemodynamic measurements in patients with mild and moderate normal-renin and low-renin essential hypertension and in age-matched normotensive subjects. In our study, compared with age-matched control subjects, normal-renin hypertensive subjects younger than 42 years with basal diastolic BPs less than 100 mm Hg had normal glomerular filtration (Cin) and effective renal plasma flow (Cpah), filtration fraction (Cin/Cpah), and renal blood flow (Cpah/1 — hematocrit value). The mean arterial pressure (MAP) and renal vascular resistance (MAP/renal blood flow) were increased. In contrast, compared with age-matched control subjects, normal-renin hypertensive subjects older than 42 years with basal diastolic BPs less than 100 mm Hg and greater than 100 mm Hg had a decreased Cpah and an increased filtration fraction. The MAP was increased, the renal blood flow decreased, and the renal vascular resistance notably increased. Subjects with low-renin essential hypertension had renal function and hemodynamic patterns indistinguishable from those of age-matched normal-renin hypertensive subjects with similar basal diastolic BPs. These data suggest that in early normal-renin essential hypertension, the increase in systemic BP is not caused by renal circulatory disturbances. Increased renal vascular resistance, however, may lead to subsequent vascular functional or structural changes, ultimately decreasing effective renal plasma flow but at a rate disproportionate to the glomerular filtration rate.

(Arch Intern Med 1982;142:1317-1323)