The use of rapid sequence mannitol pyelography in the diagnosis of renovascular hypertension.

Abstract

Ever since the association between renal vascular lesions and hypertension has been known, better tests have been sought to determine whether or not morphologically demonstrable lesions are in fact functionally significant (11, 12). Taken as a group, the rapid sequence intravenous pyelogram, the Stamey test, the Howard test, the radioactive renogram, the renal venous washout time, the renal venous renin level, and the closed renal biopsy have been fairly accurate in predicting functionally significant lesions (8–11). However, many of these tests are not simple, require special equipment, and are not readily available in the community hospital. It would seem, then, that there is great need for a safe, simple, accurate screening procedure for preliminary evaluation of patients with suspected renovascular hypertension. Presently rapid sequence intravenous pyelography and/or urea washout pyelography are widely employed as primary screening tests in the evaluation of such patients. While these methods can distinguish gross differences in renal size, subtle discrepancies in renal function are often difficult, if not impossible, to evaluate (3, 5, 6). It occurred to us that the mannitol pyelogram originally described as a modification and simplification of the drip infusion technic might have some use in screening suspected cases of renovascular hypertension since it is in fact a modified Stamey test, the only essential difference being the addition of contrast medium to the intravenous injection of osmotic diuretic and vasopressin (7). This approach seemed to offer a way of performing split renal function studies with evaluation of the roentgen findings rather than relying on occluding ureteral catheters and timed urine samples. The following case report is presented to illustrate the presumed value of the mannitol pyelogram in the evaluation of functionally significant renal vascular hypertension. Case Report A 21-year-old white male was admitted to the hospital on Nov. 27, 1966, with a chief complaint of high blood pressure. The present illness dated to December 1965, when he was first informed that he had hypertension at an Armed Forces preinduction physical examination. Since that time his blood pressure has been continually elevated. Headaches have been an occasional complaint. There was no history of renal disease, shortness of breath, or paroxysmal nocturnal dyspnea. His mother, father, and older sister all have hypertension. Physical examination revealed an alert, well developed male. The pulse was 80 and regular; the temperature 99°. The blood pressure was: sitting, right arm 165/120 and left arm 170/110; prone, right arm 160/120, left arm 170/110, and right leg 230/160. No other abnormalities were noted. Laboratory studies disclosed normal hemogram and urogram, a blood urea nitrogen of 19 mg per 100 cc, sodium 138 mEq/l, potassium 4.0 mEq/1. On Nov. 29, 1966, a modified Howard test was performed.