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(Hypertension. 2005;46:380.)
© 2005 American Heart Association, Inc.

Original Articles

Renin-Dependent Hypertension Caused by Nonfocal Stenotic Aberrant Renal Arteries

Proof of a New Syndrome

David C. Kem; Daniel F. Lyons; James Wenzl; Donald Halverstadt; Xichun Yu

From the Department of Internal Medicine (D.C.K., D.F.L., X.Y.), Cardiac Arrhythmia Research Institute (D.C.K., X.Y.), and Department of Pediatrics (J.W., D.H.) and Pediatric Urology (D.H.), University of Oklahoma Health Sciences Center and the VA Medical Center, Oklahoma City, Ok.

Correspondence to David C. Kem, MD, Professor, WP1345, 920 Stanton Young Blvd, Oklahoma City, OK 73104. E-mail david-kem{at}ouhsc.edu

We have identified 2 relatively young patients with significant hypertension, an elongated single aberrant renal artery supplying blood to a renal segment, and evidence for localization of the elevated plasma renin activity to the side and vein draining the affected kidney. Furosemide-induced diuresis and acute oral captopril stimulated the renal vein/contralateral renin ratios to 4.3:1 and 6.5:1 in patients 1 and 2, respectively. These renal vein ratios are significantly higher than normal (>3:1 under similar conditions). Partial resection of the portion of the kidney affected by the aberrant tortuous artery led to a marked reduction in blood pressure in patient 1. Patient 2, not an operative candidate, responded satisfactorily to use of a converting enzyme inhibitor, which helped to confirm the dependency of the blood pressure on the abnormal flow relationship existing within that aberrant artery and the kidney. We believe these 2 patients are representative of a small but distinct subgroup within the larger number of patients with elongated single or multiple renal aberrant arteries. Each aberrant artery had no focal stenosis, although a decrease in flow relative to the tissue perfusion demands was apparent from the marked activation of the renin-angiotensin system in the venous system draining that artery. The increased length of such vessels may contribute to their decreased flow, although their average diameter may reside just above such a critical value for a normal length vessel. This new syndrome, involving more than one component of the flow/resistance relationship, has been overlooked when renin-dependent forms of hypertension are considered.

Key Words: angiotensin • arteries • hypertension, renal • renin • vessels

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