Diagnostic Radiology
Page Kidney: An Unusual Cause of Hypertension 1 Peter L. Scott, M.D., Heun Y. Yune, M.D., and Myron H. Weinberger, M.D. A case of classical Page kidney with emphasis on radiographic findings is presented. Onset of hypertension following trauma associated with angiographic findings of attenuation, splaying and stretching of the intrarenal vessels on the arterial phase with a definite delay in transit time through the parenchyma and a non-homogeneous nephrogram should make the diagnosis of Page kidney or constricting subcapsular mass the most logical consideration. INDEX TERMS: Hypertension. Kidneys, hemorrhage. Kidneys, wounds and injuries. Veins, renal Radiology 119:547-548. June 1976
1939, Page (7) produced the first experimental perinephritic kidney. He also created hypertension in a dog, cat, and rabbit by wrapping one or both kidneys with cellophane, which produced a thick fibrocollagenous hull surrounding the kidney, leaving the renal vessels uninvolved. The resultant perinephritis began within three to five days after the procedure, with marked hypertension occurring about four to five weeks later. Hypertension occurred whether one or both kidneys were involved, consistent with current concepts of the renin-angiotensin-aldosterone system and its role in arterial pressure (2). In 1930, McKenzie (6) reported a single patient with a perinephric hematoma and hypertension who became normotensive following nephrectomy. Engle and Page (1) reported a case of hypertension in a 19-year-old man with no definite history of renal trauma except for the usual bruises encountered in high school football. Roentgenographic examination and surgery revealed a calcified capsular cyst encasing the kidney. Blood pressure returned to normal following nephrectomy. Several other unusual causes of fibrous encasement of the kidney causing first renal ischemia, then systemic hypertension, have been reported with the etiology believed to be other than blunt trauma. McKay and colleagues (5) reported a case secondary to pyelolithotomy, and Hayward (3) reported N
I
Table I:
Recumbent Upright
hypertension after pyeloplasty for severe hydronephrosis. Hellebusch at el. (4) described perinephric hematoma and hypertension following percutaneous renal biopsy, with relief atter evacuation of the hematoma. Even though numerous episodes of renal trauma, both external and internal in the form of surgical procedures occur every year, this still remains a rare complication. The radiographic and clinical manifestations of the "Page" kidney are pathognomonic and do permit accurate diagnosis if the entity is considered. CASE REPORT A 19-year-old white man was referred to the Indiana University Medical Center for evaluation and treatment of hypertension of unknown etiology. Urinalysis in the summer of 1973 showed albuminuria. The patient had fallen from a second story ladder striking the right lower chest, with resulting right upper quadrant fullness sever-
Split Renal Vein Renin Stud ies (Values in ngjmlj3 hrs) Right Renal Vein (R RV)
Left Renal Vein (LRV)
Inferior Vena Cava
55
12
270
38
12 26
(IVC)
Fig. 2. Excretory urography sequence of flush abdominal aortogram. A. There is a definite delay in visualization of calyces and renal pelvis on the patient's right side. B. Calyces on the right appear distorted and splayed, showing extrinsic pressure changes. No definite right renal outline is visualized. Fig. 3. Arterial phase of abdominal flush sequence demonstrates normal renal artery origins (arrows) arising from the aorta.
Fig. 1. Pathologic specimen of right kidney clearly shows the markedly thickened renal capsule and cyst which is open. Fibrous encasement of the kidney is seen over the renal cortex.
1 From the Department of Radiology, Indiana University Medical Center, Indianapolis, Ind. Revised manuscript accepted in November 1975. Supported in part by USPHSgrant HL 14159 (Specialized Center of Research (SCOR)-Hypertension). shan
547
548
PETER
L. SCOTT AND OTHERS
June 1976
Fig. 4. Subtraction films of selective right renal arteriogram in AP and left posterior oblique projection. A. The arterial phase shows stretching, splaying and attenuation of the intrarenal vessels, consistent with mass effect. B. Nephrogram phase demonstrated non-homogeneous stain (arrows) suggesting areas of ischemia or thinning of parenchyma in lateral aspect. C-O. This projection shows an extrarenal subcapsular mass posterolaterally (arrows). Note particularly that the middle capsular artery is being markedly separated from the parenchyma, consistent with an extrarenal subcapsular mass (open arrow). al months prior to the abnormal urinalysis. High blood pressure was first documented in January of 1974, with diastolic readings of 100-120 mm Hg and systolic of 140-160 mm Hg. His maternal grandmother had become hypertensive at 67. The patient complained of dizzy spells, frontal headaches in the evening and nocturia for six months before hospitalization. On physical examination, supine blood pressure was 150/110 mm Hg, with a normal pulse. His optic fundi showed minimal arteriovenous compression. The patient then underwent split renal vein renin studies (TABLE I). Angiography (performed prior to surgery) demonstrated a posterolateral perinephric mass and arterial and venous abnormalities very suggestive of a "Page" kidney. At surgery, an enlarged right kidney covered by a cyst filled with chocolate-colored fluid was removed. The cyst was subcapsular and had a 1-2.5mm thick wall. This cyst compressed the renal parenchyma but the renal hilar vessels were normal (Fig. 1). Microscopic sections showed chronic inflammation and marked fibrosis of the renal capsule. The pathologic findings were also consistent with those foand in the classic "Page" kidney (7). The patient's blood pressure preoperatively was 140/110 mm Hg and immediately upon ligation of the renal artery it dropped to 110/ 80 mm Hg and remained in the normotensive range throughout the postoperative period. Eighteen months following surgery, blood pressure remained at 110/70 mm Hg or lower. DISCUSSION The Page kidney has been known for a number of years as a clinical entity, but little mention of this has been made in the radiologic literature. The radiographic pattern is very characteristic when added to the appropriate clinical history. As in this case, the hypertensive patient is often young, with a history of trauma that is frequently forgotten. In this case, the rapid sequence excretory urogram was obtained during the initial phase of the angiogram (Fig. 2). Definite delay in the appearance of this collecting system on the right was noted. A large avascular mass measuring 15 X 10 em arising outside the renal parenchyma but within the renal capsule causing concavity of the adjacent parenchyma was identified. The arterial phase showed no renal artery narrowing (Goldblatt kidney) (Figs. 3 and 4) but attenuation, splaying and stretching of the intrarenal vessels of the right kidney were very prominent. A definite delay in transit time through the parenchyma was also suggestive of increased intrarenal
pressure. A non-homogeneous nephrogram suggested areas of parenchymal ischemia. The changes in the calyceal configuration, intrarenal vessels, and prolonged transit time all imply increased pressure from the subcapsular mass. This increased intrarenal pressure could have been produced by a functional type of venous obstruction from the extrinslc mass (8). The duration of the subcapsular lesion, especially in traumatic conditions, appears to affect the clinical course to the extent that nephrectomy mayor may not be necessary. Accurate clinical information may obviate the need for nephrectomy. A conservative approach such as evacuation of the hematoma may be all that is required when the diagnosis is firm and extensive fibrosis and parenchymatous involvement is absent. ADDENDUM: We have recently seen a similar case. The patient was a 24-year-old man who fell and injured his side while water skiing and became hypertensive. Again, the angiogram was very helpful in making the diagnosis of perinephric hematoma. This patient also became normotensive postoperatively but a longer followup period is needed.
REFERENCES 1. Engle WJ, Page IH: Hypertension due to renal compression resulting from subcapsular hematoma. J Urol 73;735-739, May 1955 2. Grim CE, Mullins MF, Nilson JP, et al: Unilateral "Page kidney" hypertension in man: studies of the renin-angiotensin-aldosterone system before and after nephrectomy. JAMA 231:42-45,6 Jan 1975 3 Hayward WG: Renal surgery as a cause for renal ischemia. J Urol 51:486-490, May 1944 4. Hellebusch AA, Simmons JL, Holland N: Renal ischemia and hypertension from a constrictive perirenal hematoma. JAMA 214:757-759,26 Oct 1970 5 McKay A, Proctor LD, Roome NW: Hypertension after removal of a renal calculus. Can Med Assoc J 50:328-:331, Apr 1944 6. MacKenzie OW: Perirenal hematoma primary with polycythemia. J Urol 23:535-543, May 1930 7. Page IH: The production of persistent arterial hypertension by cellophane perinephritis. JAMA 113:2046-2048, 2 Dec 1939 8. Waugh WH, Hamilton WF: Physical effects of increased venous and extrarenal pressure on renal vascular resistance. eirc Res 6:116-121, Jan 1958
Page Kidney: An Unusual Cause of Hypertension 1 Peter L. Scott, M.D., Heun Y. Yune, M.D., and Myron H. Weinberger, M.D. A case of classical Page kidney with emphasis on radiographic findings is presented. Onset of hypertension following trauma associated with angiographic findings of attenuation, splaying and stretching of the intrarenal vessels on the arterial phase with a definite delay in transit time through the parenchyma and a non-homogeneous nephrogram should make the diagnosis of Page kidney or constricting subcapsular mass the most logical consideration. INDEX TERMS: Hypertension. Kidneys, hemorrhage. Kidneys, wounds and injuries. Veins, renal Radiology 119:547-548. June 1976
1939, Page (7) produced the first experimental perinephritic kidney. He also created hypertension in a dog, cat, and rabbit by wrapping one or both kidneys with cellophane, which produced a thick fibrocollagenous hull surrounding the kidney, leaving the renal vessels uninvolved. The resultant perinephritis began within three to five days after the procedure, with marked hypertension occurring about four to five weeks later. Hypertension occurred whether one or both kidneys were involved, consistent with current concepts of the renin-angiotensin-aldosterone system and its role in arterial pressure (2). In 1930, McKenzie (6) reported a single patient with a perinephric hematoma and hypertension who became normotensive following nephrectomy. Engle and Page (1) reported a case of hypertension in a 19-year-old man with no definite history of renal trauma except for the usual bruises encountered in high school football. Roentgenographic examination and surgery revealed a calcified capsular cyst encasing the kidney. Blood pressure returned to normal following nephrectomy. Several other unusual causes of fibrous encasement of the kidney causing first renal ischemia, then systemic hypertension, have been reported with the etiology believed to be other than blunt trauma. McKay and colleagues (5) reported a case secondary to pyelolithotomy, and Hayward (3) reported N
I
Table I:
Recumbent Upright
hypertension after pyeloplasty for severe hydronephrosis. Hellebusch at el. (4) described perinephric hematoma and hypertension following percutaneous renal biopsy, with relief atter evacuation of the hematoma. Even though numerous episodes of renal trauma, both external and internal in the form of surgical procedures occur every year, this still remains a rare complication. The radiographic and clinical manifestations of the "Page" kidney are pathognomonic and do permit accurate diagnosis if the entity is considered. CASE REPORT A 19-year-old white man was referred to the Indiana University Medical Center for evaluation and treatment of hypertension of unknown etiology. Urinalysis in the summer of 1973 showed albuminuria. The patient had fallen from a second story ladder striking the right lower chest, with resulting right upper quadrant fullness sever-
Split Renal Vein Renin Stud ies (Values in ngjmlj3 hrs) Right Renal Vein (R RV)
Left Renal Vein (LRV)
Inferior Vena Cava
55
12
270
38
12 26
(IVC)
Fig. 2. Excretory urography sequence of flush abdominal aortogram. A. There is a definite delay in visualization of calyces and renal pelvis on the patient's right side. B. Calyces on the right appear distorted and splayed, showing extrinsic pressure changes. No definite right renal outline is visualized. Fig. 3. Arterial phase of abdominal flush sequence demonstrates normal renal artery origins (arrows) arising from the aorta.
Fig. 1. Pathologic specimen of right kidney clearly shows the markedly thickened renal capsule and cyst which is open. Fibrous encasement of the kidney is seen over the renal cortex.
1 From the Department of Radiology, Indiana University Medical Center, Indianapolis, Ind. Revised manuscript accepted in November 1975. Supported in part by USPHSgrant HL 14159 (Specialized Center of Research (SCOR)-Hypertension). shan
547
548
PETER
L. SCOTT AND OTHERS
June 1976
Fig. 4. Subtraction films of selective right renal arteriogram in AP and left posterior oblique projection. A. The arterial phase shows stretching, splaying and attenuation of the intrarenal vessels, consistent with mass effect. B. Nephrogram phase demonstrated non-homogeneous stain (arrows) suggesting areas of ischemia or thinning of parenchyma in lateral aspect. C-O. This projection shows an extrarenal subcapsular mass posterolaterally (arrows). Note particularly that the middle capsular artery is being markedly separated from the parenchyma, consistent with an extrarenal subcapsular mass (open arrow). al months prior to the abnormal urinalysis. High blood pressure was first documented in January of 1974, with diastolic readings of 100-120 mm Hg and systolic of 140-160 mm Hg. His maternal grandmother had become hypertensive at 67. The patient complained of dizzy spells, frontal headaches in the evening and nocturia for six months before hospitalization. On physical examination, supine blood pressure was 150/110 mm Hg, with a normal pulse. His optic fundi showed minimal arteriovenous compression. The patient then underwent split renal vein renin studies (TABLE I). Angiography (performed prior to surgery) demonstrated a posterolateral perinephric mass and arterial and venous abnormalities very suggestive of a "Page" kidney. At surgery, an enlarged right kidney covered by a cyst filled with chocolate-colored fluid was removed. The cyst was subcapsular and had a 1-2.5mm thick wall. This cyst compressed the renal parenchyma but the renal hilar vessels were normal (Fig. 1). Microscopic sections showed chronic inflammation and marked fibrosis of the renal capsule. The pathologic findings were also consistent with those foand in the classic "Page" kidney (7). The patient's blood pressure preoperatively was 140/110 mm Hg and immediately upon ligation of the renal artery it dropped to 110/ 80 mm Hg and remained in the normotensive range throughout the postoperative period. Eighteen months following surgery, blood pressure remained at 110/70 mm Hg or lower. DISCUSSION The Page kidney has been known for a number of years as a clinical entity, but little mention of this has been made in the radiologic literature. The radiographic pattern is very characteristic when added to the appropriate clinical history. As in this case, the hypertensive patient is often young, with a history of trauma that is frequently forgotten. In this case, the rapid sequence excretory urogram was obtained during the initial phase of the angiogram (Fig. 2). Definite delay in the appearance of this collecting system on the right was noted. A large avascular mass measuring 15 X 10 em arising outside the renal parenchyma but within the renal capsule causing concavity of the adjacent parenchyma was identified. The arterial phase showed no renal artery narrowing (Goldblatt kidney) (Figs. 3 and 4) but attenuation, splaying and stretching of the intrarenal vessels of the right kidney were very prominent. A definite delay in transit time through the parenchyma was also suggestive of increased intrarenal
pressure. A non-homogeneous nephrogram suggested areas of parenchymal ischemia. The changes in the calyceal configuration, intrarenal vessels, and prolonged transit time all imply increased pressure from the subcapsular mass. This increased intrarenal pressure could have been produced by a functional type of venous obstruction from the extrinslc mass (8). The duration of the subcapsular lesion, especially in traumatic conditions, appears to affect the clinical course to the extent that nephrectomy mayor may not be necessary. Accurate clinical information may obviate the need for nephrectomy. A conservative approach such as evacuation of the hematoma may be all that is required when the diagnosis is firm and extensive fibrosis and parenchymatous involvement is absent. ADDENDUM: We have recently seen a similar case. The patient was a 24-year-old man who fell and injured his side while water skiing and became hypertensive. Again, the angiogram was very helpful in making the diagnosis of perinephric hematoma. This patient also became normotensive postoperatively but a longer followup period is needed.
REFERENCES 1. Engle WJ, Page IH: Hypertension due to renal compression resulting from subcapsular hematoma. J Urol 73;735-739, May 1955 2. Grim CE, Mullins MF, Nilson JP, et al: Unilateral "Page kidney" hypertension in man: studies of the renin-angiotensin-aldosterone system before and after nephrectomy. JAMA 231:42-45,6 Jan 1975 3 Hayward WG: Renal surgery as a cause for renal ischemia. J Urol 51:486-490, May 1944 4. Hellebusch AA, Simmons JL, Holland N: Renal ischemia and hypertension from a constrictive perirenal hematoma. JAMA 214:757-759,26 Oct 1970 5 McKay A, Proctor LD, Roome NW: Hypertension after removal of a renal calculus. Can Med Assoc J 50:328-:331, Apr 1944 6. MacKenzie OW: Perirenal hematoma primary with polycythemia. J Urol 23:535-543, May 1930 7. Page IH: The production of persistent arterial hypertension by cellophane perinephritis. JAMA 113:2046-2048, 2 Dec 1939 8. Waugh WH, Hamilton WF: Physical effects of increased venous and extrarenal pressure on renal vascular resistance. eirc Res 6:116-121, Jan 1958
