CASE REPORTS
Page Kidney: Case Report and Review of the Literature Thomas R. McCune, MD, William J. Stone, MD, and Julia A. Breyer, MD • Page kidney is caused by the accumulation of blood in the perinephric or subcapsular space, resulting in compression of the involved kidney, renal ischemia, and high renin hypertension. Most patients are young hypertensives with a remote history of blunt trauma to the abdomen or back. We describe a case of acute Page kidney following a renal biopsy in a patient with underlying IgA nephropathy. In addition to the new-onset hypertension, this patient developed a significant decline in renal function due to the inability of the contralateral diseased kidney to compensate. Magnetic resonance imaging (MRI), computed tomography (CT), and ultrasound were valuable in making this diagnosis. Medical and surgical therapeutic options were considered. This report also reviews all previously described cases of Page kidney. © 1991 by the National Kidney Foundation, Inc. INDEX WORDS: Hypertension; Page kidney; ischemic renal disease.
I
N 1955, Engel and Page reported a case of hypertension associated with a renal subcapsular hematoma in a football player who had sustained blunt trauma to the flank. 1 This was the first clinical correlate to Page's 1939 study of hypertension induced in dogs by wrapping one or both kidneys in cellophane. 2 Since 1955, there have been multiple case reports of hypertension associated with either acute or chronic unilateral subcapsular or perinephric hematomas. This syndrome has been called Page kidney. Page kidney most commonly presents in healthy individuals who have new onset hypertension with a remote history of blunt trauma to the kidney. The pathogenesis of the hypertension seen with Page kidney is analogous to that described by Goldblatt et al in 1934. 3 They demonstrated that constricting the artery to one kidney would result in ischemia and the development of hypertension. 3 In Page kidney, extrinsic parenchymal compression caused unilateral renal ischemia and increased renin release by the affected kidney. Although hypertension is usual, renal insufficiency is not common in patients with a normal contralateral kidney. Page kidney represents a potentially treatable form of hypertension. 4 . 10 This report will present a case of Page kidney of unusual etiology that was associated with both hypertension and renal dysfunction. We will review all cases of Page kidney reported in the English literature, and also discuss the anatomic basis of this lesion, methods of imaging and diagnostic studies, and potential avenues of therapy.
CASE REPORT A 33-year-old white man was hospitalized for treatment of chronic osteomyelitis and evaluation of renal insufficiency. His past medical history was remarkable for third-degree burns to SO% of his body suffered 20 months before this admission. The patient noted episodes of gross hematuria over the previous 4 years, some of which had been documented in the hospital. The patient had 2+ protein and microscopic hematuria on urinalysis approximately 20 months before this admission and on multiple subsequent urinalyses. He had no history of hypertension. The record documented many previous normal blood pressure measurements. Over the previous 20 months, his serum creatinine had increased gradually from 115 ,umol/L (1.3 mgJdL) to 239 ,umol/L (2.7 mgJdL). There was no history of recent exposure to any nephrotoxic agents. The physical examination showed a well-nourished white man with extensive scarring and loss of subcutaneous fat over his entire body below T-6 and the inner aspects of both arms. Temperature was 37.9°C and blood pressure was l20/S0 mm Hg. The physical examination was otherwise unremarkable. Laboratory data on admission showed a blood urea nitrogen (BUN) of 12.5 mmol/L (35 mg/dL), serum creatinine of239 ,umol/L (2.7 mgJdL), and a serum albumin of 30 giL (3 gJ dL). The serum creatinine level had been stable for the 2 months before this admission. Urinalysis showed 1 + protein, white blood cells (WBC) 6 to S per high power field (HPF), red blood cells (RBC) too numerous to count per HPF, and no casts. The 24-hour urine protein excretion was 14 g, and the creatinine clearance was 0.S5 mL/s (51 mL/min). The hematocrit was 43%, and the platelet count was 255,000 cells/ ,ilL. Prothrombin time, partial thromboplastin time and
From the Division of Nephrology, Vanderbilt University Medical Center, Nashville Veterans Administration Medical Center, Nashville, TN. Address reprint requests to luliaA. Breyer, MD, Vanderbilt University Medical Center, S-3223 MCN, Nashville, TN 37232-23 72. © 1991 by the National Kidney Foundation, 1nc. 0272-6386/ 91/ 1805-0010$3.00/ 0
American Journal of Kidney Diseases, Vol XVIII, No 5 (November), 1991: pp 593-599
593
594 bleeding times were within normal ranges. Erythrocyte sedimentation rate was 68 mm/h. Serologic studies were negative. A renal ultrasound demonstrated two normal-sized kidneys without evidence of hydronephrosis, but showing diffuse increased echogenicity. A percutaneous renal biopsy was performed on the right kidney with ultrasonic guidance. Ultrasound of the kidney immediately postprocedure demonstrated no hematoma. The biopsy showed IgA nephropathy. Ten hours after biopsy, the patient complained of right costovertebral angle tenderness and was noted to have a decrease in hematocrit from 38% to 35% without gross hematuria. Over the next 12 hours, the hematocrit decreased to 24% and the patient was given 2U of packed RBC. An ultrasound showed the appearance of a large right perinephric hematoma (Fig lA). Computerized tomography (CT) without contrast showed a large perinephric and subcapsular hematoma measuring 8 X \0 X 15 cm (width X height X length) encasing the right kidney (Fig I B). Magnetic resonance imaging (MRI) also demonstrated the right perinephric and subcapsular hematoma, as well as patency of the right renal artery and vein (Fig I C).
McCUNE, STONE, AND BREYER Twelve hours postbiopsy, the patient developed hypertension with a blood pressure of 150/95 mm Hg. The blood pressure remained elevated despite the addition of nifedepine (60 mg/d) and propranolol (60 mg/d), and the relief of pain with narcotics. Twenty-four hours postbiopsy, the patient was noted to have an abrupt increase in serum creatinine from 239 ",moljL (2.7 mg/ dL) to 336 ",moljL (3.8 mg/dL). The creatinine clearance decreased to 0.58 mL/s (35 ml/ min). A graphic representation of his clinical course is shown in Fig 2. There was no evidence of other causes of worsening azotemia, such as obstruction, interstitial nephritis, or acute tubular necrosis. The patient was evaluated by the urologic and vascular surgery services for evacuation of the hematoma or nephrectomy. It was felt that due to his extensive cutaneous scarring, a surgical incision would not heal and that medical management would be the best approach. Since the patient was felt not to be a candidate for a nephrectomy, more invasive studies such as renal vein renins were not performed. The addition of enalapriJ to his other medications led to successful blood pressure control. Nine months postbiopsy, the patient still required antihypertensive medicines and the creatinine clearance was 0.52 mL/s (31 mL/min). Follow-up CT scan showed a calcified fibrotic right renal capsule.
Fig 1. Radiologic evaluation of postbiopsy kidney. (A) Renal ultrasound of the kidney shows subcapsular and perinephric fluid collections. (8) CT of the abdomen demonstrates a subcapsular hematoma (*) and anterior displacement of the kidney by a large perinephric hematoma. (C) MRI of the abdomen, coronal section, shows a large retroperitoneal hematoma, a large subcapsular hematoma, and a patent right renal artery. In all panels, arrows point to the hematoma.
595
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Page Kidney: Case Report and Review of the Literature Thomas R. McCune, MD, William J. Stone, MD, and Julia A. Breyer, MD • Page kidney is caused by the accumulation of blood in the perinephric or subcapsular space, resulting in compression of the involved kidney, renal ischemia, and high renin hypertension. Most patients are young hypertensives with a remote history of blunt trauma to the abdomen or back. We describe a case of acute Page kidney following a renal biopsy in a patient with underlying IgA nephropathy. In addition to the new-onset hypertension, this patient developed a significant decline in renal function due to the inability of the contralateral diseased kidney to compensate. Magnetic resonance imaging (MRI), computed tomography (CT), and ultrasound were valuable in making this diagnosis. Medical and surgical therapeutic options were considered. This report also reviews all previously described cases of Page kidney. © 1991 by the National Kidney Foundation, Inc. INDEX WORDS: Hypertension; Page kidney; ischemic renal disease.
I
N 1955, Engel and Page reported a case of hypertension associated with a renal subcapsular hematoma in a football player who had sustained blunt trauma to the flank. 1 This was the first clinical correlate to Page's 1939 study of hypertension induced in dogs by wrapping one or both kidneys in cellophane. 2 Since 1955, there have been multiple case reports of hypertension associated with either acute or chronic unilateral subcapsular or perinephric hematomas. This syndrome has been called Page kidney. Page kidney most commonly presents in healthy individuals who have new onset hypertension with a remote history of blunt trauma to the kidney. The pathogenesis of the hypertension seen with Page kidney is analogous to that described by Goldblatt et al in 1934. 3 They demonstrated that constricting the artery to one kidney would result in ischemia and the development of hypertension. 3 In Page kidney, extrinsic parenchymal compression caused unilateral renal ischemia and increased renin release by the affected kidney. Although hypertension is usual, renal insufficiency is not common in patients with a normal contralateral kidney. Page kidney represents a potentially treatable form of hypertension. 4 . 10 This report will present a case of Page kidney of unusual etiology that was associated with both hypertension and renal dysfunction. We will review all cases of Page kidney reported in the English literature, and also discuss the anatomic basis of this lesion, methods of imaging and diagnostic studies, and potential avenues of therapy.
CASE REPORT A 33-year-old white man was hospitalized for treatment of chronic osteomyelitis and evaluation of renal insufficiency. His past medical history was remarkable for third-degree burns to SO% of his body suffered 20 months before this admission. The patient noted episodes of gross hematuria over the previous 4 years, some of which had been documented in the hospital. The patient had 2+ protein and microscopic hematuria on urinalysis approximately 20 months before this admission and on multiple subsequent urinalyses. He had no history of hypertension. The record documented many previous normal blood pressure measurements. Over the previous 20 months, his serum creatinine had increased gradually from 115 ,umol/L (1.3 mgJdL) to 239 ,umol/L (2.7 mgJdL). There was no history of recent exposure to any nephrotoxic agents. The physical examination showed a well-nourished white man with extensive scarring and loss of subcutaneous fat over his entire body below T-6 and the inner aspects of both arms. Temperature was 37.9°C and blood pressure was l20/S0 mm Hg. The physical examination was otherwise unremarkable. Laboratory data on admission showed a blood urea nitrogen (BUN) of 12.5 mmol/L (35 mg/dL), serum creatinine of239 ,umol/L (2.7 mgJdL), and a serum albumin of 30 giL (3 gJ dL). The serum creatinine level had been stable for the 2 months before this admission. Urinalysis showed 1 + protein, white blood cells (WBC) 6 to S per high power field (HPF), red blood cells (RBC) too numerous to count per HPF, and no casts. The 24-hour urine protein excretion was 14 g, and the creatinine clearance was 0.S5 mL/s (51 mL/min). The hematocrit was 43%, and the platelet count was 255,000 cells/ ,ilL. Prothrombin time, partial thromboplastin time and
From the Division of Nephrology, Vanderbilt University Medical Center, Nashville Veterans Administration Medical Center, Nashville, TN. Address reprint requests to luliaA. Breyer, MD, Vanderbilt University Medical Center, S-3223 MCN, Nashville, TN 37232-23 72. © 1991 by the National Kidney Foundation, 1nc. 0272-6386/ 91/ 1805-0010$3.00/ 0
American Journal of Kidney Diseases, Vol XVIII, No 5 (November), 1991: pp 593-599
593
594 bleeding times were within normal ranges. Erythrocyte sedimentation rate was 68 mm/h. Serologic studies were negative. A renal ultrasound demonstrated two normal-sized kidneys without evidence of hydronephrosis, but showing diffuse increased echogenicity. A percutaneous renal biopsy was performed on the right kidney with ultrasonic guidance. Ultrasound of the kidney immediately postprocedure demonstrated no hematoma. The biopsy showed IgA nephropathy. Ten hours after biopsy, the patient complained of right costovertebral angle tenderness and was noted to have a decrease in hematocrit from 38% to 35% without gross hematuria. Over the next 12 hours, the hematocrit decreased to 24% and the patient was given 2U of packed RBC. An ultrasound showed the appearance of a large right perinephric hematoma (Fig lA). Computerized tomography (CT) without contrast showed a large perinephric and subcapsular hematoma measuring 8 X \0 X 15 cm (width X height X length) encasing the right kidney (Fig I B). Magnetic resonance imaging (MRI) also demonstrated the right perinephric and subcapsular hematoma, as well as patency of the right renal artery and vein (Fig I C).
McCUNE, STONE, AND BREYER Twelve hours postbiopsy, the patient developed hypertension with a blood pressure of 150/95 mm Hg. The blood pressure remained elevated despite the addition of nifedepine (60 mg/d) and propranolol (60 mg/d), and the relief of pain with narcotics. Twenty-four hours postbiopsy, the patient was noted to have an abrupt increase in serum creatinine from 239 ",moljL (2.7 mg/ dL) to 336 ",moljL (3.8 mg/dL). The creatinine clearance decreased to 0.58 mL/s (35 ml/ min). A graphic representation of his clinical course is shown in Fig 2. There was no evidence of other causes of worsening azotemia, such as obstruction, interstitial nephritis, or acute tubular necrosis. The patient was evaluated by the urologic and vascular surgery services for evacuation of the hematoma or nephrectomy. It was felt that due to his extensive cutaneous scarring, a surgical incision would not heal and that medical management would be the best approach. Since the patient was felt not to be a candidate for a nephrectomy, more invasive studies such as renal vein renins were not performed. The addition of enalapriJ to his other medications led to successful blood pressure control. Nine months postbiopsy, the patient still required antihypertensive medicines and the creatinine clearance was 0.52 mL/s (31 mL/min). Follow-up CT scan showed a calcified fibrotic right renal capsule.
Fig 1. Radiologic evaluation of postbiopsy kidney. (A) Renal ultrasound of the kidney shows subcapsular and perinephric fluid collections. (8) CT of the abdomen demonstrates a subcapsular hematoma (*) and anterior displacement of the kidney by a large perinephric hematoma. (C) MRI of the abdomen, coronal section, shows a large retroperitoneal hematoma, a large subcapsular hematoma, and a patent right renal artery. In all panels, arrows point to the hematoma.
595
PAGE KIDNEY AFTER RENAL BIOPSY
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