Goldblatt and his co-workers (1) discovered that constriction of one renal artery caused transient systemic hypertension in dogs and prolonged hypertension in other animals. Complete occlution of the renal artery did not produce this effect. Constriction of both renal arteries resulted in persistent hypertension, as did constriction of one renal artery after removal of the opposite kidney. It was also shown that hypertension could be produced by constricting the aorta proximal to the renal arteries but not by compression applied distal to these vessels. Excision of the ischemic kidney following unilateral constriction resulted in disappearance of the hypertension. Since these classical experiments, many cases of hypertension associated with constriction of a main renal artery have been reported. Among these a variety of arterial lesions has been found; all appear to have in common partial interruption of the blood flow to a kidney. These cases represent the human counterpart of Goldblatt's animal experiments. Yuile (2) classified constriction of the renal artery as of intrinsic and extrinsic origin. The intrinsic causes include embolism (3–7), thrombosis (8–12), developmental defects (13), aneurysm (14, 15), arteriosclerotic plaques (16), and syphilitic arteritis (17). Extrinsic causes are compression of the renal artery by aortic aneurysm (18), retroperitoneal tumor (19), hydatid cyst (20), organizing hematoma (21), intrarenal tumor (22), and kinking or torsion (23, 24). While the value of abdominal arteriography for the detection of these conditions has frequently been mentioned, relatively few arteriograms have been made for this purpose. In fact, there has been little effort to assess the status of the renal arteries by this means in any group of patients with hypertension, whatever the cause. In earlier reports on abdominal arteriography from the Cincinnati General Hospital (25, 26) only one of the 75 patients with hypertension showed constriction of a main renal artery. Because of this experience, we believe that arteriography has little value as a routine measure in the clinical investigation of the hypertensive patient. Moderately elevated blood pressure is not uncommon among patients suffering from thrombosis of the abdominal aorta. The explanation for this is obscure, but it is apparent from our own arteriograms and those appearing in the literature that it does not usually originate from renal artery constriction. However, upward extension of the thrombus to involve a renal artery does occur in this disease and may produce severe hypertension. To our knowledge, the demonstration of this combination of circumstances has not been previously recorded. The present report deals with 3 such cases. In each, abdominal arteriograms were available before and after the development of hypertension and vividly portrayed the changes presumably responsible for the blood pressure elevation.