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Renovascular Hypertension Developing as a Complication of Selective Renal Arteriography
Vol. 107, June Printed in U.S.A.
THE JOURNAL OF UROLOGY
Copyright © 1972 by The Williams & Wilkins Co.
RENOVASCULAR HYPERTENSION DEVELOPING AS A COMPLICATION OF SELECTIVE RENAL ARTERIOGRAPHY W. B. GILL,* A. T. COLE
AND
R. J. WONG
From the Department of Surgery (Urology), University of Chicago, Chicago, Illinois
Renovascular hypertension, the development of diastolic hypertension following partial occlusion of the renal artery, has become well accepted in principle.1 Since Goldblatt's pioneering investigations with renal artery clips in the early 1930's, 2 several clinical lesions have been found which produce narrowing of the renal artery and diastolic hypertension. Atherosclerosis in the older age groups 3 and fibromuscular dysplasia in the younger age groups4 head the list. Other less common causes of renal artery stenosis which have been reported are renal artery aneurysms, emboli, thrombi, arteritis and extrinsic tumor compressions. 5 • 6 Renovascular hypertension which developed as a complication of selective renal arteriography is described herein. CASE REPORT
This is a case report of subintimal injection of contrast material into the wall of the renal artery during selective renal arteriography which produced marked stenosis of the renal artery and subsequent hypertension. R. C., a 34-year-old man, had gross hematuria and left renal colic. A left retrograde pyelogram revealed a 1.0 cm. radiolucent filling defect in the superior calix of the left kidney. Serum uric acid, sickle cell preparation, hemoglobin electrophoresis and bleeding and clotting studies were normal. With diuresis and antibiotic therapy, the colic subsided. A repeat retrograde pyelogram 10 days later revealed a radiolucent filling defect in the Accepted for publication July 23, 1971. Read at annual meeting of American Urological Association, Chicago, Illinois, May 16-20, 1971. Supported in part by the E. F. Andrews Foundation. * Requests for reprints: 950 East 59th Street, Chicago, Illinois 60637. 1 Glenn, J. F. and Anderson, E. E.: Reversible renovascular hypertension. Ann. Rev. Med., 18: 219, 1967. 2 Goldblatt, H., Lynch, J., Hanzal, R. F. and Summerville, W.W.: Studies on experimental hypertension. I. The production of persistent elevation of systolic blood pressure by means of renal ischemia. J. Exper. Med., 69: 347, 1934. 3 Brolin, I.: Renal artery changes in hypertension. Acta Radio!., 6: 401, 1967. 4 Kincaid, 0. W., Davis, G. D., Hallermann, F. J. and Hunt, J. C.: Fibromuscular dysplasia of the renal arteries. Arteriographic features, classification, and observations on natural history of the disease. Amer. J. Roentgen., 104: 271, 1968. 6 Poutasse, E. F.: Surgical treatment of renal hypertension. Amer. J. Surg., 107: 97, 1964. 6 DeBakey, M. E., Morris, G. C., Jr., Morgen, R. 0., Crawford, E. S. and Cooley, D. A.: Lesions of the renal artery. Surgical technic and results. Amer. J. Surg., 107: 84, 1964.
left superior calix which was now 1.5 by 2 cm. Because of the suspicion of a tumor in the left kidney, a left selective renal arteriogram was obtained. The left selective renal arteriogram revealed a 5 cm. avascular mass in the upper middle area of the left kidney. The renal artery was normal. After the patient was turned for oblique views, a second injection of contrast material was made. Under fluoroscopic visualization, the angiographer noted that the test dose of dye persisted in the wall of the artery. Therefore, the complete injection was not made and the catheter was withdrawn from the renal artery. Because the angiographer was suspicious of injection into the wall of the renal artery, an aortogram was made. The aortogram revealed almost complete occlusion of the left renal artery 1.5 cm. from its origin, which corresponded to the site at which the selective catheter tip had been a few minutes before (fig. 1). Dull aching pain persisted in the left flank area for the first day and definite diastolic hypertension was observed as early as 4 hours after the arteriogram. The blood pressure ranged from 150/95 to 200/115 mm. Hg during the next 8 days, with the majority of the diastolic readings being more than 100 mm. Hg. The elevated blood pressure was recorded in both arms, both legs and in all positions (lying, sitting and standing). The patient had been
Fm. 1. Aortogram made shortly after left selective renal arteriogram shows almost complete occlusion of left renal artery (arrow). 922
RENOVASCULAR HYPERTENSION
923
Retrograde dijj erential renal function studies Volume (ml./10 min.) Right kidney urine Left kidney urine Bladder urine
41
1.5 0.25
Na+ (mEq./L)
Creatinine (mg.%)
32
19
20 41
33
17
normotensive prior to the arteriogram and was without a history of hypertension. Retrograde differential renal function studies were performed 7 days after the arteriogram. After passing number 7 whistle-tip ureteral catheters to both renal pelves and establishing oral hydration, IO-minute urine collections were made during the ensuing hour (see table). These results of decreased volume, decreased sodium concentration and increased creatinine concentration in the urine from the kidney with renal artery stenosis indicated that the lesion was a functional one, producing diastolic hypertension. 7 The serum lactate dehydrogenase (LDH) rose from a pre-arteriogram normal level of 45 to 245 units per cent on the second post-arteriogram day, which was further evidence of acute renal ischemia. 8 The patient was taken to the operating room 9 days after the arteriogram had been made. There were 2 reasons for operation: an avascular parenchymal mass and a persistent filling defect suggestive of an avascular hypernephroma and marked diastolic hypertension secondary to an iatrogenic renal artery stenosis. Exploration of the left renal vessels and parenchyma was done through a left subcostal transperitoneal incision. The left renal artery did not have a pulse distal to the proximal 1 cm. The renal artery contained a firm mass within the lumen from a point 1 cm. from the origin with the aorta extending down the artery approximately 1.5 cm. Intra-arterial pressure measurements with a 20-gauge needle connected to a strain gauge revealed a blood pressure of 150 /100 in the aorta and proximal 1 cm. of the left renal artery. In the distal left renal artery the pressure was 20/15 mm. Hg. The left renal artery exploration and arterial pressure measurements confirmed the preoperative diagnosis of left renal artery stenosis secondary to thrombosis from intramural injection of angiographic contrast material. After the renal vessels were occluded with vascular clamps and the splenic flexure was reflected, a firm mass was readily palpable through Gerota's fascia in the upper pole of the left kidney. Because this mass was most likely a renal cell carcinoma coupled with a severe renal artery stenosis, we proceeded with radical nephrectomy. The blood pressure returned to normotensive levels on the first postoperative day and has remained normal during the ensuing 15 months. 7 Howard, J. E. and Connor, T. B.: Use of differential renal function studies in the diagnosis of renovascular hypertension. Amer. J. Surg., 107: 58, 1964. 8 Sakati, I. A., Devine, P. C., Devine, C. J., Jr., Fiveash, J. G., Jr. and Poutasse, E. F.: Serum lactic dehydrogenase in acute renal infarction and ischemia. New Engl. J. Med., 278: 721, 1968.
Fm. 2. Gross specimen with opened left renal artery shows hematoma elevating intima.
Fm. 3. Photomicrograph of renal artery wall organizing hematoma lying primarily between and adventitia. Arrow to adventitial side at site of upheaval of intima and media. Reduced from X20.
924
GILL, COLE AND WONG PATHOLOGY FINDINGS
The left renal artery was filled with a blue mass measuring approximately 1.5 cm. long (fig. 2). When the left renal artery was opened this mass was found to be an intramural hematoma with the intima appearing intact over it. The lumen of the artery was narrowed to 2 mm. by this intramural hematoma. Microscopically the hematoma was in the adventitia and was covered by media and intima on its luminal surface (fig. 3). Early organization was evident at the margins. In the kidney there were several small areas of infarction at the periphery. The upper pole of the kidney contained a 3.5 cm. yellow tumor with the center appearing grayish and somewhat necrotic. This mass had eroded through the superior major calix for about 1.5 cm., which produced the radiolucent filling defect on the urogram. No venous invasion was seen. The kidney capsule was intact over the tumor. Microscopic examination of the tumor revealed its center to be largely necrotic but its borders showed the typical pattern of a renal tubular cell adenocarcinoma. Periaortic lymph nodes revealed no evidence of tumor. DISCUSSION
We believe that this is the first documented report of renovascular hypertension developing as a complication of renal arteriography. In 1969 Robertson reviewed 1,750 cases of renal angiography and did not report this complication nor did he allude to its possibility. 9 Evidence that the renal artery stenosis was functionally related to the development of diastolic hypertension includes the following: 1) sudden onset approximately 4 hours after the creation of the renal artery stenosis, 2) retrograde differential renal function studies showed the typical pattern of functional 9 Robertson, P. W., Dyson, M. L. and Sutton, P. D.: Renal angiography. A review of 1750 cases. Clin. Radiol., 20: 401, 1969.
renal artery stenosis (decreased urine volume, decreased sodium concentration and increased creatinine concentration), 3) marked intra-arterial pressure drop measured across the stenosis at operation, 4) acute elevation of serum LDH following the stenosis8 and 5) return and maintenance of normotension following nephrectomy. If it were not for the associated hypernephroma in this case a reparative renovascular operation would have had to be considered. With the increasing use of renal arteriography this complication of injection into the arterial wall will undoubtedly be seen with increasing frequency. Our case clearly demonstrates that intramural injection of contrast material during selective renal arteriography can produce significant renal artery stenosis and diastolic hypertension. This entity will have to be considered as another possible cause of renovascular hypertension and a potential indication for reparative renovascular surgery. SUMMARY
A case is reported of the injection of radiographic contrast material into the wall of the renal artery during selective renal arteriography which produced marked stenosis of the renal artery and subsequent diastolic hypertension. Functional proof of renovascular hypertension was obtained from retrograde differential renal function studies and the intraarterial pressure drop across the stenosis measured at operation. Nephrectomy was performed primarily because of an associated hypernephroma, and the patient became normotensive and has remained so now for the 15 months of followup. Histologic study confirmed marked stenosis of the renal artery by a 1.5 by 0.5 cm. intramural (adventitial-medial) organizing hematoma. Intramural injection of contrast material during renal angiography will now have to be considered as a possible cause of renovascular hypertension and a potential indication for reparative renovascular surgery.
THE JOURNAL OF UROLOGY
Copyright © 1972 by The Williams & Wilkins Co.
RENOVASCULAR HYPERTENSION DEVELOPING AS A COMPLICATION OF SELECTIVE RENAL ARTERIOGRAPHY W. B. GILL,* A. T. COLE
AND
R. J. WONG
From the Department of Surgery (Urology), University of Chicago, Chicago, Illinois
Renovascular hypertension, the development of diastolic hypertension following partial occlusion of the renal artery, has become well accepted in principle.1 Since Goldblatt's pioneering investigations with renal artery clips in the early 1930's, 2 several clinical lesions have been found which produce narrowing of the renal artery and diastolic hypertension. Atherosclerosis in the older age groups 3 and fibromuscular dysplasia in the younger age groups4 head the list. Other less common causes of renal artery stenosis which have been reported are renal artery aneurysms, emboli, thrombi, arteritis and extrinsic tumor compressions. 5 • 6 Renovascular hypertension which developed as a complication of selective renal arteriography is described herein. CASE REPORT
This is a case report of subintimal injection of contrast material into the wall of the renal artery during selective renal arteriography which produced marked stenosis of the renal artery and subsequent hypertension. R. C., a 34-year-old man, had gross hematuria and left renal colic. A left retrograde pyelogram revealed a 1.0 cm. radiolucent filling defect in the superior calix of the left kidney. Serum uric acid, sickle cell preparation, hemoglobin electrophoresis and bleeding and clotting studies were normal. With diuresis and antibiotic therapy, the colic subsided. A repeat retrograde pyelogram 10 days later revealed a radiolucent filling defect in the Accepted for publication July 23, 1971. Read at annual meeting of American Urological Association, Chicago, Illinois, May 16-20, 1971. Supported in part by the E. F. Andrews Foundation. * Requests for reprints: 950 East 59th Street, Chicago, Illinois 60637. 1 Glenn, J. F. and Anderson, E. E.: Reversible renovascular hypertension. Ann. Rev. Med., 18: 219, 1967. 2 Goldblatt, H., Lynch, J., Hanzal, R. F. and Summerville, W.W.: Studies on experimental hypertension. I. The production of persistent elevation of systolic blood pressure by means of renal ischemia. J. Exper. Med., 69: 347, 1934. 3 Brolin, I.: Renal artery changes in hypertension. Acta Radio!., 6: 401, 1967. 4 Kincaid, 0. W., Davis, G. D., Hallermann, F. J. and Hunt, J. C.: Fibromuscular dysplasia of the renal arteries. Arteriographic features, classification, and observations on natural history of the disease. Amer. J. Roentgen., 104: 271, 1968. 6 Poutasse, E. F.: Surgical treatment of renal hypertension. Amer. J. Surg., 107: 97, 1964. 6 DeBakey, M. E., Morris, G. C., Jr., Morgen, R. 0., Crawford, E. S. and Cooley, D. A.: Lesions of the renal artery. Surgical technic and results. Amer. J. Surg., 107: 84, 1964.
left superior calix which was now 1.5 by 2 cm. Because of the suspicion of a tumor in the left kidney, a left selective renal arteriogram was obtained. The left selective renal arteriogram revealed a 5 cm. avascular mass in the upper middle area of the left kidney. The renal artery was normal. After the patient was turned for oblique views, a second injection of contrast material was made. Under fluoroscopic visualization, the angiographer noted that the test dose of dye persisted in the wall of the artery. Therefore, the complete injection was not made and the catheter was withdrawn from the renal artery. Because the angiographer was suspicious of injection into the wall of the renal artery, an aortogram was made. The aortogram revealed almost complete occlusion of the left renal artery 1.5 cm. from its origin, which corresponded to the site at which the selective catheter tip had been a few minutes before (fig. 1). Dull aching pain persisted in the left flank area for the first day and definite diastolic hypertension was observed as early as 4 hours after the arteriogram. The blood pressure ranged from 150/95 to 200/115 mm. Hg during the next 8 days, with the majority of the diastolic readings being more than 100 mm. Hg. The elevated blood pressure was recorded in both arms, both legs and in all positions (lying, sitting and standing). The patient had been
Fm. 1. Aortogram made shortly after left selective renal arteriogram shows almost complete occlusion of left renal artery (arrow). 922
RENOVASCULAR HYPERTENSION
923
Retrograde dijj erential renal function studies Volume (ml./10 min.) Right kidney urine Left kidney urine Bladder urine
41
1.5 0.25
Na+ (mEq./L)
Creatinine (mg.%)
32
19
20 41
33
17
normotensive prior to the arteriogram and was without a history of hypertension. Retrograde differential renal function studies were performed 7 days after the arteriogram. After passing number 7 whistle-tip ureteral catheters to both renal pelves and establishing oral hydration, IO-minute urine collections were made during the ensuing hour (see table). These results of decreased volume, decreased sodium concentration and increased creatinine concentration in the urine from the kidney with renal artery stenosis indicated that the lesion was a functional one, producing diastolic hypertension. 7 The serum lactate dehydrogenase (LDH) rose from a pre-arteriogram normal level of 45 to 245 units per cent on the second post-arteriogram day, which was further evidence of acute renal ischemia. 8 The patient was taken to the operating room 9 days after the arteriogram had been made. There were 2 reasons for operation: an avascular parenchymal mass and a persistent filling defect suggestive of an avascular hypernephroma and marked diastolic hypertension secondary to an iatrogenic renal artery stenosis. Exploration of the left renal vessels and parenchyma was done through a left subcostal transperitoneal incision. The left renal artery did not have a pulse distal to the proximal 1 cm. The renal artery contained a firm mass within the lumen from a point 1 cm. from the origin with the aorta extending down the artery approximately 1.5 cm. Intra-arterial pressure measurements with a 20-gauge needle connected to a strain gauge revealed a blood pressure of 150 /100 in the aorta and proximal 1 cm. of the left renal artery. In the distal left renal artery the pressure was 20/15 mm. Hg. The left renal artery exploration and arterial pressure measurements confirmed the preoperative diagnosis of left renal artery stenosis secondary to thrombosis from intramural injection of angiographic contrast material. After the renal vessels were occluded with vascular clamps and the splenic flexure was reflected, a firm mass was readily palpable through Gerota's fascia in the upper pole of the left kidney. Because this mass was most likely a renal cell carcinoma coupled with a severe renal artery stenosis, we proceeded with radical nephrectomy. The blood pressure returned to normotensive levels on the first postoperative day and has remained normal during the ensuing 15 months. 7 Howard, J. E. and Connor, T. B.: Use of differential renal function studies in the diagnosis of renovascular hypertension. Amer. J. Surg., 107: 58, 1964. 8 Sakati, I. A., Devine, P. C., Devine, C. J., Jr., Fiveash, J. G., Jr. and Poutasse, E. F.: Serum lactic dehydrogenase in acute renal infarction and ischemia. New Engl. J. Med., 278: 721, 1968.
Fm. 2. Gross specimen with opened left renal artery shows hematoma elevating intima.
Fm. 3. Photomicrograph of renal artery wall organizing hematoma lying primarily between and adventitia. Arrow to adventitial side at site of upheaval of intima and media. Reduced from X20.
924
GILL, COLE AND WONG PATHOLOGY FINDINGS
The left renal artery was filled with a blue mass measuring approximately 1.5 cm. long (fig. 2). When the left renal artery was opened this mass was found to be an intramural hematoma with the intima appearing intact over it. The lumen of the artery was narrowed to 2 mm. by this intramural hematoma. Microscopically the hematoma was in the adventitia and was covered by media and intima on its luminal surface (fig. 3). Early organization was evident at the margins. In the kidney there were several small areas of infarction at the periphery. The upper pole of the kidney contained a 3.5 cm. yellow tumor with the center appearing grayish and somewhat necrotic. This mass had eroded through the superior major calix for about 1.5 cm., which produced the radiolucent filling defect on the urogram. No venous invasion was seen. The kidney capsule was intact over the tumor. Microscopic examination of the tumor revealed its center to be largely necrotic but its borders showed the typical pattern of a renal tubular cell adenocarcinoma. Periaortic lymph nodes revealed no evidence of tumor. DISCUSSION
We believe that this is the first documented report of renovascular hypertension developing as a complication of renal arteriography. In 1969 Robertson reviewed 1,750 cases of renal angiography and did not report this complication nor did he allude to its possibility. 9 Evidence that the renal artery stenosis was functionally related to the development of diastolic hypertension includes the following: 1) sudden onset approximately 4 hours after the creation of the renal artery stenosis, 2) retrograde differential renal function studies showed the typical pattern of functional 9 Robertson, P. W., Dyson, M. L. and Sutton, P. D.: Renal angiography. A review of 1750 cases. Clin. Radiol., 20: 401, 1969.
renal artery stenosis (decreased urine volume, decreased sodium concentration and increased creatinine concentration), 3) marked intra-arterial pressure drop measured across the stenosis at operation, 4) acute elevation of serum LDH following the stenosis8 and 5) return and maintenance of normotension following nephrectomy. If it were not for the associated hypernephroma in this case a reparative renovascular operation would have had to be considered. With the increasing use of renal arteriography this complication of injection into the arterial wall will undoubtedly be seen with increasing frequency. Our case clearly demonstrates that intramural injection of contrast material during selective renal arteriography can produce significant renal artery stenosis and diastolic hypertension. This entity will have to be considered as another possible cause of renovascular hypertension and a potential indication for reparative renovascular surgery. SUMMARY
A case is reported of the injection of radiographic contrast material into the wall of the renal artery during selective renal arteriography which produced marked stenosis of the renal artery and subsequent diastolic hypertension. Functional proof of renovascular hypertension was obtained from retrograde differential renal function studies and the intraarterial pressure drop across the stenosis measured at operation. Nephrectomy was performed primarily because of an associated hypernephroma, and the patient became normotensive and has remained so now for the 15 months of followup. Histologic study confirmed marked stenosis of the renal artery by a 1.5 by 0.5 cm. intramural (adventitial-medial) organizing hematoma. Intramural injection of contrast material during renal angiography will now have to be considered as a possible cause of renovascular hypertension and a potential indication for reparative renovascular surgery.