At her nephrology visit, her BPtru measurement was 127/84 mm Hg on 10 mg of amlopidine. She had elevated renin (10.8 µg/L/h) and it was unclear if the high renin was secondary to amlodipine use or from renal vascular hypertension given that she had mild FMD on CT or activation of the renin-angiotensin system from renal ischemia induced from coiling of her AVMs, possibly resulting in a clinical analog of the experimental Page kidney. The patient was switched to metoprolol as she also had complaints of palpitations. In addition, 24-hour urine was collected for her ureteral stone workup.

Her 24-hour urine study revealed adequate urine volume of 2,730 cc, calcium excretion of 286.8 mg, citric acid excretion of 434 mg, sodium excretion of 159 mmol, and uric acid excretion of 488.2 mg. There was slightly increased oxalate excretion of 52 mg. The patient was instructed to adhere to a low oxalate diet.

Six months following her initial presentation, the patient’s BP was well controlled on metoprolol 50 mg daily. Her renin levels decreased to 1.8 µg/L/hr. She has not had a recurrence of nephrolithiasis.

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Although the definitive diagnosis of a Page kidney would ideally demonstrate lateralization of renin to the right kidney with bilateral renal vein renin measurements, the patient’s clinical scenario is very suggestive of a Page kidney causing hypertension because her BP improved after she was started on medication that blocked the renin-aldosterone system.


In 1939, Irvine Page described a cause of arterial hypertension by wrapping canine kidneys in cellophane, which induced renal ischemia. Once the cellophane was removed or the kidney was resected, BP improved.1

Page kidney has been described as arterial hypertension caused by extrinsic compression of the kidney, leading to microvascular ischemia. This model of hypertension differs from the Goldblatt model, where the major renal vessels are compressed, leading to renovascular hypertension.2 Extrinsic compression of the kidney can be the result of trauma, post-operative changes, hematomas, or mass lesions.2

More recently, Page kidney has been described in  percutaneous allograft renal biopsy, in which post-biopsy complications included a rise in BP and a rise in serum creatinine accompanied by elevated resistive indices on Doppler study and ultrasound of transplanted kidneys showing large subcapsular perinephric hematoma. Treatment included surgical intervention with evacuation of the hematoma, resulting in rapid improvement of BP and serum creatinine to baseline.3 It is important to recognize Page kidney as a cause of hyperreninemic hypertension that can be potentially reversible as compression to the kidney is alleviated.

The authors are affiliated with the Cleveland Clinic’s Glickman Urological and Kidney Institute.


  1. Page, IH. The production of persistent arterial hypertension by cellophage perinephritis. JAMA 1939;113:2046-2048.
  2. Dopson, SJ, Jayakumar S. Page Kidney as a rare cause of hypertension: case report and review of the literature. Am J Kidney Dis 2009;54:334-339.
  3. Posadas, MA, Muhammad BH. Acute renal failure and severe hypertension from a Page kidney post-transplant biopsy. The Scientific World Journal 2010;10:1539-1542.