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The Page Kidney: A Correctable form of Arterial Hypertension
Vol. 113, April
THE JOURNAL OF UROLOGY
Printed in U.S.~..
Copyright © 1975 by The Williams & Wilkins Co.
THE PAGE KIDNEY: A CORRECTABLE FORM OF ARTERIAL HYPERTENSl01'-f GERALD SUFRIN* From the James Buchanan Brady Urological Institute, The Johns Hopkins Hospital, Baltimore, Maryland
In 1836 Bright observed an association between renal disease and hypertension.' However, it was not until 1934 when Goldblatt and associates demonstrated that systemic arterial hypertension could be produced by constricting the renal artery that renewed interest in the relation between the kidney and hypertension occurred. 2 Subsequently, Page was able to produce arterial hypertension by inducing a fibrous perinephritis. 3 The Page kidney then refers to that form of hypertension caused by compression of the renal parenchyma itself by a perirenal process. The main renal vessels by definition are uninvolved. Page demonstrated further that either removal of the compressive force around such a kidney or nephrectomy would ameliorate the hypertension. Clinically a larger number of patients with hypertension caused by renal artery lesions have been identified than those owing to mechanisms outlined by Page. Indeed only about 27 documented cases of the Page kidney have been reported and many of these were documented prior to the availability of newer diagnostic tests, such as divided function studies, selective arteriography and renal vein renin determinations. •- 10 Herein are Accepted for publication July 5, 1974. * Current address: Roswell Park Memorial Institute 666 Elm Street, Buffalo, New York 14203. ' 1 Bright: Causes and observations, illustrative of renal disease accompanied with the secretion of albuminous urine. Guys Hosp. Rep., 1: 338, 1836. 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. Exp. Med., 59: 347, 1934. • Page, I. H.: The production of persistent arterial hypertension by cellophane perinephritis. J.A.M.A., 113: 2046, 1939. 'Massumi, R. A., Andrade, A. and Kramer, N.: Arterial hypertension in traumatic subcapsular perirenal hematoma (Page kidney). Evidence for renal ischemia. Amer. J. Med., 46: 635, 1969. 'Martin, K. W.: Spontaneous circumrenal haematoma; review and report of•2 cases. Brit. Med. J. 1: 1118, 1949. ' "Hellebusch, A. A., Simmons, J. L. and Holland, N.: Renal ischemia and hypertension from a constrictive perirenal hematoma. J.A.M.A., 214: 757, 1970. 7 Grant, R. P., Jr., Gifford, R. W., Jr., Pudvan, W.R., Meaney, T. F., Straffon, R. A. and McCormack, L. J.: Renal trauma and hypertension. Amer. J. Cardiol., 27: 173, 1971. "Marshall, W. H., Jr. and Castellino, R. A.: Hypertension produced by constricting capsular renal lesions ("Page" kidney). Radiology, 101: 561, 1971. •sos, T. A., Niceta, P., Levin, D. C. and Baltaxe, H. A.: Perinephric masses-a cause of renovascular hypertension. Clin. Radio!., 24: 464, 1973. 10 Jameson, R. M.: Transient hypertension associated with closed renal injury. Brit. J. Urol., 45: 482, 1973. 450
reported 2 cases of Page kidney, emphasiz~·g functional and radiographic correlations. The lit rature is reviewed and a therapeutic plan is s ggested. I 1
CASE REPORTS
1
Case 1. F. W. D., JHH 150-36-22, a20-year-~ld man known to be normotensive, was struck in tp.e right flank by a lacrosse stick 12 months prior Ito hospitalization. There was no hematuria and otjly moderate flank discomfort, which subsided af~er several days. The patient was entirely asymp~omatic when he was noted to be hypertensive bn routine physical examination a month prior [to hospitalization. He was on no medication ahd there was no history of renal disease. Famhy history was non-contributory. Blood pressure was 180/120 with the pati~nt supine and pulse was 84. Examination was normal except for a non-tender right flank mass t~at moved with respiration. No bruits were hea~d. Complete blood count, urinalysis and all ot~er laboratory studies were normal. An excretory urogram (IVP) showed a large mass flattening the lateral aspect of the right kidrnfy, distorting the collecting system and displacing t~e kidney and collecting system medially (fig. 1, A) .l A B-mode sonogram revealed a cystic mass lateraljto the right kidney (fig. 1, B). A selective right rerial arteriogram showed a renal artery of normal c~liber with splaying of the intraparenchymal vess~ls by a mass lateral to the kidney (fig. 2). Capsular vessels extended around the mass with stainingiof the capsule in the nephrographic phase. Also, flattening of the lateral aspect of the kidney Wias seen. Divided function studies and renal vein retiin determinations indicated that the right kidney "'1as responsible for the hypertension (table 1). At the operation a right subcapsular cyst \\jas evacuated and decorticated with the release of 6bO ml. hemosiderin containing fluid of the followi~g composition: sodium 142 mEq. per 1., chloride 1p4 mEq. per 1., potassium 3. 7 mEq. per 1., urea 15 n:j.g. per cent, total protein 4. 7 gm. per cent and calcium 8.7 mg. per cent. The fibrous base of the dst remained on the kidney. Histologic study of the cyst wall showed fibrous tissue with foci of organlzing hematoma. A year postoperatively the patiE1~t still required 75 mg. hydrochlorothiazide daily Ito maintain a blood pressure of 135/90. Case 2. R. H., JHH 141-93-21, a previom(ly healthy 16-year-old boy, suffered severe biparietal headaches unrelated to activity or position i 3 months prior to hospitalization. There were ho other symptoms. The history was negative for
!
451
PAGE KIDNEY
FIG. 1. Case 1. A, IVP shows flattening of lateral aspect of right kidney, with distortion and displacement medially of kidney and collecting system. B, sonogram shows cystic mass lateral to right kidney.
trauma, urinary tract infection or hematuria. Family history was negative for renal disease and hypertension. Blood pressure was 160/110 with the patient supine and pulse was 82. Examination was normal and no flank masses or abdominal bruits were noted. All laboratory studies were normal. An IVP showed a large mass in the right kidney with splaying, medial displacement and distortion of the collecting system. A selective right renal arteriogram demonstrated a renal artery of normal caliber but splaying of the intraparenchymal vessels (fig. 3, A). No tumor vessels were seen. A prominent capsular artery, separated from the parenchyma by an avascular mass, extended around the upper and lateral aspects of this mass. A later phase shows staining of the capsule and flattening of the lateral border of the kidney (fig. 3, B). Divided function studies were positive on the right side (table 1). A right nephrectomy was performed. The specimen showed a subcapsular hematoma with marked compression and thinning of the renal parenchyma. The wall of the collection consisted of fibrous tissue 4 mm. thick. A year postoperatively blood pressure was 130/76 without medication. REVIEW OF THE LITERATURE
male patients. While a history of blunt trauma, commonly contact sports and accidents, was elicited in 78 per cent of the cases only 41 per cent had gross hematuria and 4 per cent microscopic hematuria; 55 per cent had neither gross nor microscopic hematuria. The interval between a presumed etiologic event and the discovery of hypertension varied widely from 24 hours to 12 years but was generally less than 1 year. When commented on, a flank mass was palpable in about half of the cases. The proximate cause, that is the pathologic process producing the Page kidney, was equally divided between subcapsular and perirenal masses compressing the kidney. Although 85 per cent of these masses were surgically documented to be secondary to hemorrhage, that is either subcapsular or perirenal hematomas, subcapsular or perirenal urinomas were also seen (15 per cent). Regardless of composition the volume of these collections was usually in excess of 500 ml. Unaccountably the right kidney was involved more commonly than the left. Diagnostic evaluation depended on an IVP or retrograde pyelography. However, the availability of arteriography, sonography and renin determinations would seem to contribute further to diagnostic precision. Treatment has included nephrectomy (59 per cent), observation (27 per cent) or drainage and decortication (14 per cent).
Previously reported cases of the Page kidney are summarized. 4-1o The average age of these patients was 25 years and 89 per cent of the cases involved
The Page kidney results when fluid (blood or urine) is contained under pressure within either
DISCUSSION
452
SUFRIN
Fm. 2. Case 1. Selective right renal arteriogram shows renal artery of normal caliber with splaying of intraparenchymal vessel.
the subcapsular or perirenal space, thereby constricting the renal parenchyma. Figure 4 illustrates the pertinent anatomy. The renal capsule, which strips easily from the underlying normal kidney by blunt dissection or fluid under pressure, forms the outer boundary of the potential subcapsular space. The perirenal space is between the renal capsule and Gerota's fascia. Although not perfectly watertight, it is only when fluid accumulates within the perirenal or subcapsular space that sufficient parenchymal tamponade can occur to produce the Page kidney. This fact has been documented previously4-1° and by the 2 cases reported herein. External to Gerota's fascia is the pararenal space which is contiguous with the general retroperitoneum. Fluid collections here are unlikely to produce renal tamponade since they expand into the entire retroperitoneum. Page observed that constriction of the renal parenchyma itself without compromise of the main renal vessels altered intrarenal hemodynamics to produce renal ischemia and hypertension. 3 The mechanism whereby compression of the renal parenchyma cau~es hypertension was demonstrated by Waugh and Hamilton. 11 They observed that while extrinsic compression of the parenchyma produced a fall in intrarenal arterial and intrarenal venous pressure, the decrease in arterial pressure 11 Waugh, W. H. and Hamilton, W. F.: Physical effects of increased venous and extrarenal pressure on renal vascular resistance. Circ. Res., 6: 116, 1958.
was greater. This decrease in pressure results in a decrease in renal blood flow and most significantly a reduction in mean renal perfusion pressure. A decrease in mean renal perfusion pressure is a primary determinant of renin release leading to the formation of angiotensin 2 and systemic arterial hypertension. 12 Renin substrate or angiotensinogen is a glycoprotein synthesized by the liver and present in the alpha 2 globulin fraction of the plasma. Renin that is secreted by the juxtaglomerular cells of the kidney in response to decreased perfusion pressure acts on renin substrate to produce the decapeptide angiotensin 1. Converting enzyme present in the lung and kidney cleaves the phenylalanine-histidine bond of angiotensin 1 to give the octapeptide angiotensin 2, a highly potent vasopressor 40 times as active as norepinephrine. Angiotensin 2 is degraded by the angiotensina,se system consisting of aminopeptidases, endopeptidases and carboxypeptidases to inactive peptides and amino acids. 12 The excretory pattern of an ischemic kidney when compared to normal includes a decreased urine volume and sodium concentration and an increase in urinary creatinine concentration. 13 Evidence that the mechanism of arterial hypertension in the Page kidney is associated with unilateral renal ischemia is seen in the divided function studies of the cases herein reported (table 1) and in the reports of Schroeder, and Massumi and associates.• Furthermore, it has been documented that the ischemic Page kidney secretes excessive amounts of renin. In general and irrespective of absolute values a renal vein renin ratio between the normal and ischemic kidney of 1 to 1.5 or greater is functionally significant and implicates the ischemic kidney as the cause of hypertension. 14, 15 In case 1 and in the reports of Schroeder, and Sos and associates• the renal vein renin determinations between the ischemic Page kidney and the normal kidney satisfy this criterion. Thus, as Page observed, although renal ischemia is produced by a method different from clamping of the main renal vessels the basic mechanism for the production of hypertension is the same. 3 Depending on the location of the encysted fluid collection, the limiting membrane may or may not have an epithelial lining. In the latter event a pseudocapsule forms as a result of fibrosis of the 12 Pickering, G.: High Blood Pressure, 2nd ed. New York: Grune & Stratton, Inc., p. 105, 1968. 13 Maxwell, M. H., Lupu, A. N. and Kaufman, J. J.: Individual kidney function tests in renal arterial hypertension. J. Urol., 100: 384, 1968. "Michelakis, A. M., Foster, J. H., Liddle, G. W., Rhamy, R. K., Kuchel, 0. and Gordon, R. D.: Measurement of renin in both renal veins. Its use in diagnosis of renovascular hypertension. Arch. Intern. Med., 120: 444, 1967. 15 Winer, B. M., Lubbe, W. F., Simon, M. and Williams, J. A.: Renin in the diagnosis of renovascular hypertension. Activity in renal and peripheral vein plasma. J.A.M.A., 202: 121, 1967.
453
PAGE KIDNEY TABLE
1. Divided renal function studies Case 1
Rt. Urine volume (ml./min.) Urine sodium (mEq./1.) Urine creatinine (mg./100 ml.) Renal vein renin ratio rt./lt.
Case 2 Lt.
4.5 ± 1.3 86 ± 3.3 13 ± .57
0.86 ± .03 17 ± 1.2 45 ± 3.7
1.5
Rt.
Lt.
1.4 ± .7 10.3 ± .3 15 ± 2.0 191 ± 19.0 37.5 ± 8.5 99.5 ± 19.0 Not obtained
Values are mean of 3 determinations plus or minus standard error of mean.
FIG. 3. Case 2. A, selective right renal arteriogram illustrates prominent capsular artery separated from parenchyma by avascular mass. Normal size renal artery with splaying of intraparenchymal vessels is also seen. B, nephrogram phase of selective arteriogram shows capsular staining.
----- PARARENAL SPACE
FIG. 4. Schematic illustration of perirenal spaces
surrounding tissue. Analysis of the contained subcapsular or perirenal fluid often shows evidence of hemorrhage, either grossly or by the presence of hemosiderin. Moreover, study of the cyst fluid as in case 1 showed its composition to be similar to that
of serum. Indeed Marshall and Castellino investigated the dynamics of the limiting membrane in the case of a subcapsular hematoma and concluded that the fluid contained within the cyst was not fixed and unchanged from the time of trauma but participated in at least simple membrane diffusion.• It is well to emphasize that although most of the reported cases of the Page kidney have been associated with a history of trauma other cases of subcapsular or perirenal bleeding, such as neoplasm, hemorrhagic diathesis, polyarteritis, angiomyolipoma, percutaneous renal biopsy or anticoagulation therapy, could cause the Page kidney effect. In any event if the fluid is under sufficient pressure to tamponade the renal parenchyma, hypertension will result. Generally, the radiologic manifestations of the Page kidney are those of the underlying condition producing the Page kidney. Most commonly this is either a subcapsular or a perirenal hematoma of size sufficient to compress the renal parenchyma.
454
SUFRIN TABLE
2. Radiographic findings in subcapsular and perirenal hematomas * Subcapsular Hematoma
Perirenal Hematoma
Plainx-ray
Outline of kidney and retroperitoneal structures are preserved Renal silhouette is enlarged but maintains reniform configuration
Soft tissue mass in retroperitoneum Renal outline and psoas margins are indistinct Renal axis is displaced anteromedially Kidney is relathzely immobile and does not move with respiration
IVP
Collecting system is usually displaced medially and is disproportionally smaller than renal silhouette Renal surface flattened beneath hematoma
Direction of collecting system is variable but usually anteromedial Medial deviation of ureter Renal surface not flattened
Arteriogram
Capsular artery is displaced laterally but maintains normal close relation to capsule Elevated renal capsule visualized
Capsular artery may be displaced from parenchyma and capsule Renal capsule not visualized
* Modified from Pollack and Popky." TABLE
Nephrectomy Decortication and evacuation Observation Combined results
3. Methods and results of treatment of the Page kidney Total Cases Treated(%)
Av.PreTreatment B.P. (mm.Hg)
Av. PostTreatment B.P. (mm.Hg)
Cured or Improved* No. (%)
59 14 27 100
174/112 170/112 160/112 169/112
126/76 143/95 131/86 130/82
15 ofl7 (88) 2of4 (50) 7 of8 (88) 24 of29 (82)
Unimproved No. (%) 2ofl7 2of4 1 of8 5 of29
(12) (50) (12) (18)
* Reduction of blood pressure to 140/90, without medication for at least 1 year.''
Pollack and Popky recently reviewed the radiologic manifestations of subcapsular and perirenal hematomas and table 2 summarizes these observations. 16 High dose urography with tomography as well as arteriography are essential and permit accurate diagnosis. In addition ultrasound and percutaneous cyst puncture offer new approaches to diagnosis. Table 3, which includes all previously reported cases and the 2 cases reported herein summarizes the results of therapy. Treatment of the Page kidney has included nephrectomy, decortication and evacuation of a subcapsular or perirenal collection, or merely observation. None of the last 2 groups required subsequent nephrectomy, emphasizing that if spontaneous resorption fails to occur prompt relief of compression before irreversible damage occurs may allow renal preservation. The success of expectant treatment in 27 per cent of cases emphasizes that a constricting perirenal or subcapsular hematoma producing hypertension can reabsorb with remission of hypertension.•, 10 Should reabsorption fail to occur and should hypertension persist after a reasonable period of medical management, an operation is indicated to ameliorate hypertension and preserve renal function. Clearly, evacuation and decortication of the cyst best achieve these objectives. Delay may allow organization of a fibrous hull on the kidney itself as in the first case. 1 •Pollack, H. M. and Popky, G. L.: Roentgenographic manifestations of spontaneous renal hemorrhage. Radiology, 110: 1, 1974.
If the patient is seen when hypertension cannot be controlled and renal salvage impossible, then unilateral nephrectomy is necessary. Here the excellent results achieved (88 per cent cured or improved) may be contrasted to cases in whi!ch nephrectomy was performed for hypertension associated with an apparent unilateral renal abnormality. An extensive review of such cases by Smith revealed only a 26 per cent rate of cure or improvement. ' 7 SUMMARY
The Page kidney is a remediable form of renal hypertension. It is usually seen in young male patients with an antecedent history of blunt renal trauma, followed by a subcapsular or perirel)al hematoma causing compression of the renal parenchyma and hypertension. Radiographic studies demonstrate the presence of an extrinsic mass compressing the kidney. Divided function studies and renal vein renin determinations confirm the functional significance of this process in the etiology of hypertension. Treatment may initially consist of observation. However, if hypertension persists then decortication and evacuation of the encysted fluid are indicated. In long-standing cases, although nephrectomy may be necessary, the chance of relieving hypertension is excellent. Dr. R. M. E. Engel permitted the study of case 1 and Dr. W.W. Scott permitted the study of case 2. 17 Smith, H. W.: Unilateral nephrectomy in hypertensive disease. J. Urol., 76: 685, 1956.
THE JOURNAL OF UROLOGY
Printed in U.S.~..
Copyright © 1975 by The Williams & Wilkins Co.
THE PAGE KIDNEY: A CORRECTABLE FORM OF ARTERIAL HYPERTENSl01'-f GERALD SUFRIN* From the James Buchanan Brady Urological Institute, The Johns Hopkins Hospital, Baltimore, Maryland
In 1836 Bright observed an association between renal disease and hypertension.' However, it was not until 1934 when Goldblatt and associates demonstrated that systemic arterial hypertension could be produced by constricting the renal artery that renewed interest in the relation between the kidney and hypertension occurred. 2 Subsequently, Page was able to produce arterial hypertension by inducing a fibrous perinephritis. 3 The Page kidney then refers to that form of hypertension caused by compression of the renal parenchyma itself by a perirenal process. The main renal vessels by definition are uninvolved. Page demonstrated further that either removal of the compressive force around such a kidney or nephrectomy would ameliorate the hypertension. Clinically a larger number of patients with hypertension caused by renal artery lesions have been identified than those owing to mechanisms outlined by Page. Indeed only about 27 documented cases of the Page kidney have been reported and many of these were documented prior to the availability of newer diagnostic tests, such as divided function studies, selective arteriography and renal vein renin determinations. •- 10 Herein are Accepted for publication July 5, 1974. * Current address: Roswell Park Memorial Institute 666 Elm Street, Buffalo, New York 14203. ' 1 Bright: Causes and observations, illustrative of renal disease accompanied with the secretion of albuminous urine. Guys Hosp. Rep., 1: 338, 1836. 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. Exp. Med., 59: 347, 1934. • Page, I. H.: The production of persistent arterial hypertension by cellophane perinephritis. J.A.M.A., 113: 2046, 1939. 'Massumi, R. A., Andrade, A. and Kramer, N.: Arterial hypertension in traumatic subcapsular perirenal hematoma (Page kidney). Evidence for renal ischemia. Amer. J. Med., 46: 635, 1969. 'Martin, K. W.: Spontaneous circumrenal haematoma; review and report of•2 cases. Brit. Med. J. 1: 1118, 1949. ' "Hellebusch, A. A., Simmons, J. L. and Holland, N.: Renal ischemia and hypertension from a constrictive perirenal hematoma. J.A.M.A., 214: 757, 1970. 7 Grant, R. P., Jr., Gifford, R. W., Jr., Pudvan, W.R., Meaney, T. F., Straffon, R. A. and McCormack, L. J.: Renal trauma and hypertension. Amer. J. Cardiol., 27: 173, 1971. "Marshall, W. H., Jr. and Castellino, R. A.: Hypertension produced by constricting capsular renal lesions ("Page" kidney). Radiology, 101: 561, 1971. •sos, T. A., Niceta, P., Levin, D. C. and Baltaxe, H. A.: Perinephric masses-a cause of renovascular hypertension. Clin. Radio!., 24: 464, 1973. 10 Jameson, R. M.: Transient hypertension associated with closed renal injury. Brit. J. Urol., 45: 482, 1973. 450
reported 2 cases of Page kidney, emphasiz~·g functional and radiographic correlations. The lit rature is reviewed and a therapeutic plan is s ggested. I 1
CASE REPORTS
1
Case 1. F. W. D., JHH 150-36-22, a20-year-~ld man known to be normotensive, was struck in tp.e right flank by a lacrosse stick 12 months prior Ito hospitalization. There was no hematuria and otjly moderate flank discomfort, which subsided af~er several days. The patient was entirely asymp~omatic when he was noted to be hypertensive bn routine physical examination a month prior [to hospitalization. He was on no medication ahd there was no history of renal disease. Famhy history was non-contributory. Blood pressure was 180/120 with the pati~nt supine and pulse was 84. Examination was normal except for a non-tender right flank mass t~at moved with respiration. No bruits were hea~d. Complete blood count, urinalysis and all ot~er laboratory studies were normal. An excretory urogram (IVP) showed a large mass flattening the lateral aspect of the right kidrnfy, distorting the collecting system and displacing t~e kidney and collecting system medially (fig. 1, A) .l A B-mode sonogram revealed a cystic mass lateraljto the right kidney (fig. 1, B). A selective right rerial arteriogram showed a renal artery of normal c~liber with splaying of the intraparenchymal vess~ls by a mass lateral to the kidney (fig. 2). Capsular vessels extended around the mass with stainingiof the capsule in the nephrographic phase. Also, flattening of the lateral aspect of the kidney Wias seen. Divided function studies and renal vein retiin determinations indicated that the right kidney "'1as responsible for the hypertension (table 1). At the operation a right subcapsular cyst \\jas evacuated and decorticated with the release of 6bO ml. hemosiderin containing fluid of the followi~g composition: sodium 142 mEq. per 1., chloride 1p4 mEq. per 1., potassium 3. 7 mEq. per 1., urea 15 n:j.g. per cent, total protein 4. 7 gm. per cent and calcium 8.7 mg. per cent. The fibrous base of the dst remained on the kidney. Histologic study of the cyst wall showed fibrous tissue with foci of organlzing hematoma. A year postoperatively the patiE1~t still required 75 mg. hydrochlorothiazide daily Ito maintain a blood pressure of 135/90. Case 2. R. H., JHH 141-93-21, a previom(ly healthy 16-year-old boy, suffered severe biparietal headaches unrelated to activity or position i 3 months prior to hospitalization. There were ho other symptoms. The history was negative for
!
451
PAGE KIDNEY
FIG. 1. Case 1. A, IVP shows flattening of lateral aspect of right kidney, with distortion and displacement medially of kidney and collecting system. B, sonogram shows cystic mass lateral to right kidney.
trauma, urinary tract infection or hematuria. Family history was negative for renal disease and hypertension. Blood pressure was 160/110 with the patient supine and pulse was 82. Examination was normal and no flank masses or abdominal bruits were noted. All laboratory studies were normal. An IVP showed a large mass in the right kidney with splaying, medial displacement and distortion of the collecting system. A selective right renal arteriogram demonstrated a renal artery of normal caliber but splaying of the intraparenchymal vessels (fig. 3, A). No tumor vessels were seen. A prominent capsular artery, separated from the parenchyma by an avascular mass, extended around the upper and lateral aspects of this mass. A later phase shows staining of the capsule and flattening of the lateral border of the kidney (fig. 3, B). Divided function studies were positive on the right side (table 1). A right nephrectomy was performed. The specimen showed a subcapsular hematoma with marked compression and thinning of the renal parenchyma. The wall of the collection consisted of fibrous tissue 4 mm. thick. A year postoperatively blood pressure was 130/76 without medication. REVIEW OF THE LITERATURE
male patients. While a history of blunt trauma, commonly contact sports and accidents, was elicited in 78 per cent of the cases only 41 per cent had gross hematuria and 4 per cent microscopic hematuria; 55 per cent had neither gross nor microscopic hematuria. The interval between a presumed etiologic event and the discovery of hypertension varied widely from 24 hours to 12 years but was generally less than 1 year. When commented on, a flank mass was palpable in about half of the cases. The proximate cause, that is the pathologic process producing the Page kidney, was equally divided between subcapsular and perirenal masses compressing the kidney. Although 85 per cent of these masses were surgically documented to be secondary to hemorrhage, that is either subcapsular or perirenal hematomas, subcapsular or perirenal urinomas were also seen (15 per cent). Regardless of composition the volume of these collections was usually in excess of 500 ml. Unaccountably the right kidney was involved more commonly than the left. Diagnostic evaluation depended on an IVP or retrograde pyelography. However, the availability of arteriography, sonography and renin determinations would seem to contribute further to diagnostic precision. Treatment has included nephrectomy (59 per cent), observation (27 per cent) or drainage and decortication (14 per cent).
Previously reported cases of the Page kidney are summarized. 4-1o The average age of these patients was 25 years and 89 per cent of the cases involved
The Page kidney results when fluid (blood or urine) is contained under pressure within either
DISCUSSION
452
SUFRIN
Fm. 2. Case 1. Selective right renal arteriogram shows renal artery of normal caliber with splaying of intraparenchymal vessel.
the subcapsular or perirenal space, thereby constricting the renal parenchyma. Figure 4 illustrates the pertinent anatomy. The renal capsule, which strips easily from the underlying normal kidney by blunt dissection or fluid under pressure, forms the outer boundary of the potential subcapsular space. The perirenal space is between the renal capsule and Gerota's fascia. Although not perfectly watertight, it is only when fluid accumulates within the perirenal or subcapsular space that sufficient parenchymal tamponade can occur to produce the Page kidney. This fact has been documented previously4-1° and by the 2 cases reported herein. External to Gerota's fascia is the pararenal space which is contiguous with the general retroperitoneum. Fluid collections here are unlikely to produce renal tamponade since they expand into the entire retroperitoneum. Page observed that constriction of the renal parenchyma itself without compromise of the main renal vessels altered intrarenal hemodynamics to produce renal ischemia and hypertension. 3 The mechanism whereby compression of the renal parenchyma cau~es hypertension was demonstrated by Waugh and Hamilton. 11 They observed that while extrinsic compression of the parenchyma produced a fall in intrarenal arterial and intrarenal venous pressure, the decrease in arterial pressure 11 Waugh, W. H. and Hamilton, W. F.: Physical effects of increased venous and extrarenal pressure on renal vascular resistance. Circ. Res., 6: 116, 1958.
was greater. This decrease in pressure results in a decrease in renal blood flow and most significantly a reduction in mean renal perfusion pressure. A decrease in mean renal perfusion pressure is a primary determinant of renin release leading to the formation of angiotensin 2 and systemic arterial hypertension. 12 Renin substrate or angiotensinogen is a glycoprotein synthesized by the liver and present in the alpha 2 globulin fraction of the plasma. Renin that is secreted by the juxtaglomerular cells of the kidney in response to decreased perfusion pressure acts on renin substrate to produce the decapeptide angiotensin 1. Converting enzyme present in the lung and kidney cleaves the phenylalanine-histidine bond of angiotensin 1 to give the octapeptide angiotensin 2, a highly potent vasopressor 40 times as active as norepinephrine. Angiotensin 2 is degraded by the angiotensina,se system consisting of aminopeptidases, endopeptidases and carboxypeptidases to inactive peptides and amino acids. 12 The excretory pattern of an ischemic kidney when compared to normal includes a decreased urine volume and sodium concentration and an increase in urinary creatinine concentration. 13 Evidence that the mechanism of arterial hypertension in the Page kidney is associated with unilateral renal ischemia is seen in the divided function studies of the cases herein reported (table 1) and in the reports of Schroeder, and Massumi and associates.• Furthermore, it has been documented that the ischemic Page kidney secretes excessive amounts of renin. In general and irrespective of absolute values a renal vein renin ratio between the normal and ischemic kidney of 1 to 1.5 or greater is functionally significant and implicates the ischemic kidney as the cause of hypertension. 14, 15 In case 1 and in the reports of Schroeder, and Sos and associates• the renal vein renin determinations between the ischemic Page kidney and the normal kidney satisfy this criterion. Thus, as Page observed, although renal ischemia is produced by a method different from clamping of the main renal vessels the basic mechanism for the production of hypertension is the same. 3 Depending on the location of the encysted fluid collection, the limiting membrane may or may not have an epithelial lining. In the latter event a pseudocapsule forms as a result of fibrosis of the 12 Pickering, G.: High Blood Pressure, 2nd ed. New York: Grune & Stratton, Inc., p. 105, 1968. 13 Maxwell, M. H., Lupu, A. N. and Kaufman, J. J.: Individual kidney function tests in renal arterial hypertension. J. Urol., 100: 384, 1968. "Michelakis, A. M., Foster, J. H., Liddle, G. W., Rhamy, R. K., Kuchel, 0. and Gordon, R. D.: Measurement of renin in both renal veins. Its use in diagnosis of renovascular hypertension. Arch. Intern. Med., 120: 444, 1967. 15 Winer, B. M., Lubbe, W. F., Simon, M. and Williams, J. A.: Renin in the diagnosis of renovascular hypertension. Activity in renal and peripheral vein plasma. J.A.M.A., 202: 121, 1967.
453
PAGE KIDNEY TABLE
1. Divided renal function studies Case 1
Rt. Urine volume (ml./min.) Urine sodium (mEq./1.) Urine creatinine (mg./100 ml.) Renal vein renin ratio rt./lt.
Case 2 Lt.
4.5 ± 1.3 86 ± 3.3 13 ± .57
0.86 ± .03 17 ± 1.2 45 ± 3.7
1.5
Rt.
Lt.
1.4 ± .7 10.3 ± .3 15 ± 2.0 191 ± 19.0 37.5 ± 8.5 99.5 ± 19.0 Not obtained
Values are mean of 3 determinations plus or minus standard error of mean.
FIG. 3. Case 2. A, selective right renal arteriogram illustrates prominent capsular artery separated from parenchyma by avascular mass. Normal size renal artery with splaying of intraparenchymal vessels is also seen. B, nephrogram phase of selective arteriogram shows capsular staining.
----- PARARENAL SPACE
FIG. 4. Schematic illustration of perirenal spaces
surrounding tissue. Analysis of the contained subcapsular or perirenal fluid often shows evidence of hemorrhage, either grossly or by the presence of hemosiderin. Moreover, study of the cyst fluid as in case 1 showed its composition to be similar to that
of serum. Indeed Marshall and Castellino investigated the dynamics of the limiting membrane in the case of a subcapsular hematoma and concluded that the fluid contained within the cyst was not fixed and unchanged from the time of trauma but participated in at least simple membrane diffusion.• It is well to emphasize that although most of the reported cases of the Page kidney have been associated with a history of trauma other cases of subcapsular or perirenal bleeding, such as neoplasm, hemorrhagic diathesis, polyarteritis, angiomyolipoma, percutaneous renal biopsy or anticoagulation therapy, could cause the Page kidney effect. In any event if the fluid is under sufficient pressure to tamponade the renal parenchyma, hypertension will result. Generally, the radiologic manifestations of the Page kidney are those of the underlying condition producing the Page kidney. Most commonly this is either a subcapsular or a perirenal hematoma of size sufficient to compress the renal parenchyma.
454
SUFRIN TABLE
2. Radiographic findings in subcapsular and perirenal hematomas * Subcapsular Hematoma
Perirenal Hematoma
Plainx-ray
Outline of kidney and retroperitoneal structures are preserved Renal silhouette is enlarged but maintains reniform configuration
Soft tissue mass in retroperitoneum Renal outline and psoas margins are indistinct Renal axis is displaced anteromedially Kidney is relathzely immobile and does not move with respiration
IVP
Collecting system is usually displaced medially and is disproportionally smaller than renal silhouette Renal surface flattened beneath hematoma
Direction of collecting system is variable but usually anteromedial Medial deviation of ureter Renal surface not flattened
Arteriogram
Capsular artery is displaced laterally but maintains normal close relation to capsule Elevated renal capsule visualized
Capsular artery may be displaced from parenchyma and capsule Renal capsule not visualized
* Modified from Pollack and Popky." TABLE
Nephrectomy Decortication and evacuation Observation Combined results
3. Methods and results of treatment of the Page kidney Total Cases Treated(%)
Av.PreTreatment B.P. (mm.Hg)
Av. PostTreatment B.P. (mm.Hg)
Cured or Improved* No. (%)
59 14 27 100
174/112 170/112 160/112 169/112
126/76 143/95 131/86 130/82
15 ofl7 (88) 2of4 (50) 7 of8 (88) 24 of29 (82)
Unimproved No. (%) 2ofl7 2of4 1 of8 5 of29
(12) (50) (12) (18)
* Reduction of blood pressure to 140/90, without medication for at least 1 year.''
Pollack and Popky recently reviewed the radiologic manifestations of subcapsular and perirenal hematomas and table 2 summarizes these observations. 16 High dose urography with tomography as well as arteriography are essential and permit accurate diagnosis. In addition ultrasound and percutaneous cyst puncture offer new approaches to diagnosis. Table 3, which includes all previously reported cases and the 2 cases reported herein summarizes the results of therapy. Treatment of the Page kidney has included nephrectomy, decortication and evacuation of a subcapsular or perirenal collection, or merely observation. None of the last 2 groups required subsequent nephrectomy, emphasizing that if spontaneous resorption fails to occur prompt relief of compression before irreversible damage occurs may allow renal preservation. The success of expectant treatment in 27 per cent of cases emphasizes that a constricting perirenal or subcapsular hematoma producing hypertension can reabsorb with remission of hypertension.•, 10 Should reabsorption fail to occur and should hypertension persist after a reasonable period of medical management, an operation is indicated to ameliorate hypertension and preserve renal function. Clearly, evacuation and decortication of the cyst best achieve these objectives. Delay may allow organization of a fibrous hull on the kidney itself as in the first case. 1 •Pollack, H. M. and Popky, G. L.: Roentgenographic manifestations of spontaneous renal hemorrhage. Radiology, 110: 1, 1974.
If the patient is seen when hypertension cannot be controlled and renal salvage impossible, then unilateral nephrectomy is necessary. Here the excellent results achieved (88 per cent cured or improved) may be contrasted to cases in whi!ch nephrectomy was performed for hypertension associated with an apparent unilateral renal abnormality. An extensive review of such cases by Smith revealed only a 26 per cent rate of cure or improvement. ' 7 SUMMARY
The Page kidney is a remediable form of renal hypertension. It is usually seen in young male patients with an antecedent history of blunt renal trauma, followed by a subcapsular or perirel)al hematoma causing compression of the renal parenchyma and hypertension. Radiographic studies demonstrate the presence of an extrinsic mass compressing the kidney. Divided function studies and renal vein renin determinations confirm the functional significance of this process in the etiology of hypertension. Treatment may initially consist of observation. However, if hypertension persists then decortication and evacuation of the encysted fluid are indicated. In long-standing cases, although nephrectomy may be necessary, the chance of relieving hypertension is excellent. Dr. R. M. E. Engel permitted the study of case 1 and Dr. W.W. Scott permitted the study of case 2. 17 Smith, H. W.: Unilateral nephrectomy in hypertensive disease. J. Urol., 76: 685, 1956.