Use of contrast media in the recognition of hypertension of renal origin.

Abstract

There are two major types of hypertension: primary hypertension, in which the etiology is still indeterminate, and the much rarer secondary hypertension, the result of renal, endocrine, neurologic, or cardiovascular disturbances. In this latter group the etiology may be clinically demonstrable even though the details of the pressor mechanism involved are still incompletely understood. We are principally concerned here with the problem of renal hypertension and its evaluation by roentgenologic methods, with particular reference to the use of retroperitoneal contrast studies. Renal hypertension may be divided into two types—first, that developing secondary to primary renal disease and, secondly, the much less common type developing as a result of renal circulatory disturbance. A variety of primary kidney diseases may be accompanied by hypertension: I. Infections (a) Glomerulonephritis (b) Pyonephrosis (c) Tuberculosis II. Obstructive Uropathy (a) Renal Calculus (b) Hydronephrosis III. Neoplasia (a) Solitary Cysts (b) Malignant Neoplasm IV. Congenital Abnormalities (a) Polycystic Disease (b) Hypoplasia By far the most common type of hypertension in the first group is that developing as a result of glomerulonephritis. Pyonephrosis, tuberculosis, obstructive uropathy, neoplasia, and congenital abnormalities all have been responsible for hypertension in well documented cases. Occasionally when the disease is unilateral, surgical extirpation of the involved kidney may result in dramatic improvement of the patient. Since the classic experimental demonstration by Goldblatt in 1934, in which he produced definite hypertension secondary to interference with renal circulation in dogs, at least 45 similar cases have been reported in man. It is now generally accepted that interference with the circulation of all or a portion of a kidney may definitely produce hypertension. Two main forms of interference have been described. A very rare form is that resulting from pressure on the major renal artery by extrinsic sources. Aortic aneurysms and retroperitoneal tumors are the prime offenders. Intrinsic disturbance of the renal circulation producing secondary hypertension is somewhat less rare than interference as a result of pressure on the major vessels but is still quite unusual. The common causes of interference with circulation resulting in renal hypertension are (a) embolism, (b) thrombosis, (c) developmental defects (fibrous intimal proliferation), (d) arteriosclerotic plaques, (e) aneurysm, and (f) syphilitic arteritis. This type of renal hypertension is well illustrated by a case seen in our institution. Case Report A 36-year-old white male was admitted to the Veterans Administration Hospital, Philadelphia, in February 1953, because of intermittent right flank pain of one and a half years duration, which had become worse ten days prior to admission. The blood pressure was 210/126 mm. of mercury.