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Hyperreninemic hypertension secondary to a spontaneous perinephric subcapsular hematoma. An association with polyarteritis nodosa and the syndrome of a Page kidney.
T. J. Pintar, M.D., (Associate), Chief Medical Resident, University of Wisconsin Madison Medical School.
Polyarteritis nodosa (PAN) is a systemic illness of unknown etiology. Manifestations are secondary to inflammation and necrotizing vasculitis of small-medium sized vessels in multiple organ systems. Hyperreninemic hypertension has been described in the setting of PAN, though not in the setting of spontaneous renal aneurysm rupture with formation of a subcapsular perinephric hematoma. A syndrome analogous to the original description of cellophane perinephritis by Page in 1939. Page kidney is a rare cause of hyperreninemic hypertension. It most commonly presents in young, healthy individuals as a sequelae of blunt trauma to the kidney. A resulting unilateral subcapsular hematoma or encasing fibrous capsule causes extrinsic parenchymal compression. Renal cortical ischemia, increased renin release, and decline in GER by the affected kidney present as new onset severe hypertension, pain, and infrequently declining renal function.
CASE - A 25 y.o. man presented to an outside hospital with an acute onset severe right-sided flank and abdominal pain, fever, hypertension, hematuria, leukocytosis and hypokalemia. The patient had been well until seven months prior to presentation when he noted gradual onset of 25# weight loss, fatigue, migratory arthralgia and low back pain, headache and testicular pain. He denied cough, nausea, vomiting, diarrhea or dysuria. There was no history of recent pharyngitis or cellulitis. He denied other neurologic complaints or prior history of nephrolithiasis. He admitted to intravenous drug use in the preceding year, and had been involved in a motor vehicle accident seven months earlier. Initial work-up was significant for hypokalemia (K+ 2.7), leukocytosis (WBC 21,000) and urinalysis with an active sediment, sterile pyuria and no casts. Serum creatinine, BUN, and liver function tests were normal. Blood and urine cultures showed no growth. Tests for ANA, HIV, complement, ANCA, and ASO titer were normal. A PPD was negative with appropriate response to control antigens. Right upper quadrant ultrasound showed a fluid collection in the superior pole of the right kidney with no obstruction. CT scan of the abdomen revealed a right subcapsular perinephric hematoma with evidence of bilateral striated cortical attenuation. Selective renal-celiac angiogram showed multiple microaneurysms in the left and right renal and hepatic arteries consistent with a systemic vasculitis. Testing for hepatitis was consistent with an acute hepatitis B infection. Supine aldosterone and plasma renin activity were elevated and selective renal vein renin ratio was 3:2 localizing to the right kidney.
The patient received treatment with ACE inhibitors, corticosteroids and antivirals. Gradual resolution of the right subcapsular hematoma and therapy for systemic vasculitis correlated with improved blood pressure control and resolution of electrolyte abnormalities.
DISCUSSION - Polyarteritis nodosa is a systemic necrotizing vasculitis of unknown etiology. Association with hepatitis B antigenemia and immune complex induced inflammation has been described. Aneurysmal dilation of small and medium sized vessels along with renal, gastrointestinal and a host of constitutional symptoms is common. Hyperreninemic hypertension in association with renal parenchymal ischemia has been described in PAN. We report a case of compressive perinephritis caused by rupture of a subcapsular renal artery in a patient with PAN; the syndrome of a Page kidney.
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