Three ‘Pages’ in a chapter of accidents

Rashed S. Bakri1, Matthew Prime1, Ali Haydar2, Jonathan Glass3 and David J. A. Goldsmith4

1 Department of Nephrology, 3 Department of Urology and 4 Renal Unit, Guy’s and St Thomas’ NHS Trust, London, UK and 2 American University Hospital of Beirut, Lebanon

Correspondence and offprint requests to: Dr David Goldsmith, FRCP, Consultant Nephrologist, Renal Unit, Guy’s Hospital, London SE1 9RT, UK. Email: david.goldsmith{at}gstt.sthames.nhs.uk

Keywords: acute renal failure; haematoma; lithotripsy; Page kidney; transplantation



   Introduction
 Top
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
Secondary hypertension is responsible for ~5–10% of causes of hypertension in the general population [1,2]. It is rarely possible to reverse/cure secondary hypertension, but if the patient is relatively young, and the causation of the raised blood pressure is diagnosed early enough a cure can be effected. This is most typically after renal arterial intervention for fibromuscular dysplasia, or after removal of an endocrinologically active tumour.

We describe three cases of a rare cause of secondary hypertension (sometimes as here with acute renal failure), the ‘Page kidney’, where there is sustained renal parenchymal compression leading to ischaemia and activation of the renin–angiotensin–aldosterone systems. We then discuss the definition and pathophysiology of the ‘Page kidney’ phenomenon [3]. In addition, we include a mini-review of the literature regarding the reported causes, diagnostic tests and treatment.



   Case 1
 Top
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
A 35-year-old female developed focal segmental glomerulosclerosis (FSGS) presenting as nephrotic syndrome in 1983. Four years later (1987), she had progressed to end-stage renal disease and was treated with continuous ambulatory peritoneal dialysis (CAPD). A first renal transplant in 1989 failed in 1996 with recurrent FSGS. She underwent a second renal transplant in January 1997 but there was delayed graft function and four episodes of early cellular rejection. Other complications included a pulmonary embolus and urinary tract infections.

After one renal transplant biopsy under ultrasound guidance there was anuria, pain over the graft and mild hypertension. An initial ultrasound showed little to note, although Doppler signals from the renal parenchyma were sparse. The next day another renal transplant ultrasound showed an 8 x 7 cm hyperechoic region in the renal hilum consistent with a haematoma contained within the capsule (Figure 1). CT scanning confirmed a large subcapsular haematoma and renal transplant compression. Nuclear perfusion scanning showed a moderately perfused, poorly functioning kidney. Arteriography showed a faint nephrogram, and displaced renal arterial branches.



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Fig. 1. Ultrasound showing haematoma. The arrow points to an echogenic area (haematoma).

 
As a result of these investigations the patient was taken to theatre for exploration of the renal transplant—at capsulotomy a mature haematoma (400 ml) was liberated. The patient’s renal function subsequently improved to dialysis independence, and the blood pressure returned to normal. Sadly the allograft failed within 12 months due to recurrent FSGS.



   Case 2
 Top
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
The patient was a 49-year-old female with a 30-year history of type I diabetes. She developed diabetic retinopathy and proteinuria after 12 years, and reached end-stage renal failure in 1997 for which she underwent CAPD and later haemodialysis.

She opted to undergo a simultaneous kidney and pancreas transplant. Whilst the pancreas worked immediately and the patient became independent of insulin, this was not so with the kidney, which suffered delayed graft function, requiring dialysis. Immunosuppression was with prednisolone, azathioprine and tacrolimus.

A kidney biopsy was undertaken which showed acute tubular necrosis with some evidence of tacrolimus toxicity, which was in keeping with the high blood level.

There was post-biopsy discomfort, and she became mildly hypertensive (160/90 from 130/80 mmHg). Over the next couple of days her urine output, which had been >1500 ml of urine daily, declined sharply to ~200 ml/day, and her serum creatinine increased more rapidly. A renal transplant ultrasound showed a subcapsular haematoma compressing the kidney. She returned to theatre on May 10 and a large subcapsular haematoma was evacuated (from a pink and still perfused transplant), a further kidney biopsy was taken, and this showed acute tubular necrosis with no rejection. Her blood pressure returned to normal.

Around the end of the third week her serum creatinine started to fall on a daily basis, eventually achieving a plateau creatinine value of 120 µmol/l. Both organs continue to function well.



   Case 3
 Top
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
A 53-year-old man, who had undergone a traumatic right nephrectomy aged 21 years, suffered acute left-sided colic as a result of urinary calculus in the upper two-thirds of his ureter causing renal obstruction. He had a ureteric stent inserted and then was treated with two sessions of lithotripsy (Storz Modulith SL 20, 3000 shocks, Power level 600 Bar) 3 weeks apart to his solitary left kidney. After the second session the patient experienced severe pain, and there was a significant fall in haemoglobin (3 g/dl). Urine output fell, and plasma creatinine rose from 89 to 312 µmol/l in 3 days. Blood pressure rose from 130/80 to 170/80 mmHg.

Ultrasound was of limited value because of the patient’s build but it did show medial displacement of the left kidney due to a haematoma, and the absence of normal renal parenchymal blood perfusion. A CT scan of the abdomen revealed thickening of the fascial planes and a subcapsular renal haematoma extending into the pelvis (Figure 2); the lower end of the stent was coiled up in the distal ureter. The haematoma (600 ml) was surgically drained, after which urine volume, renal function and blood pressure all normalized rapidly.



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Fig. 2. Abdominal CT scan showing large renal haemotoma after lithotripsy. The arrow points to a large haematoma, which compresses normal renal tissue (see faint nephrogram).

 


   Discussion
 Top
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 
In 1939, Page published his experiment of induced hypertension where he wrapped a canine kidney with cellophane [3] and described an intense inflammatory reaction to this foreign material producing constrictive perinephritis, compression of the kidney parenchyma and hypertension. Page proved that extirpating the affected kidney could cure this high blood pressure. Page’s observations were experimental until 1955 when he reported a case of an American football player who suffered a blunt injury to the kidney producing renal haematoma and renin-mediated hypertension [4]. From then on cases of hypertension secondary to kidney compression were referred to in the literature as ‘Page’ kidney.

Pathophysiologically any external compression of the kidney can cause renal hypoperfusion and ischaemia, which activates the renin–angiotensin–aldosterone axis resulting in excess salt and water retention ultimately leading to hypertension. As the capsule of the kidney is thick and tight, even a small amount of blood in the subcapsular space can cause significant renal ischaemia (as can other causes of renal swelling, e.g. pyelonephritis).

There are about 75 cases of Page kidney reported in the literature secondary to various diseases. Most of the cases are secondary to bleeding either into the subcapsular space or between the kidneys and surrounding tissue. However, it can be spontaneous as in polyarteritis nodosa, haemodialysis patient with acquired cysts. It is reported as complicating lithotripsy, kidney biopsy, sympathetic nerve block and trauma [59]. Table 1 lists these diverse aetiologies.


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Table 1. Causes of Page kidney

 
All imaging modalities have been tried to diagnose Page kidney. Ultrasound is the simplest approach but can miss small compressive subcapsular haematomas. CT of the abdomen is the commonest imaging modality used for diagnosis. MRI has the advantage of estimating the age of haematomas, which has therapeutic implications. Renal arteriography can be used to evaluate vascular tears and also renal parenchymal injury [10].

Treatment of Page kidney is controversial and depends on many factors. The aim of any modality of treatment or procedure is to try to spare the kidney and to cure the hypertension. In the era of modern potent anti-hypertensive drugs, particularly ACE inhibitors and angiotensin receptor blockers, the haemodynamic effect of the haematoma secondary to activation of the renin–angiotensin system can now be blocked. The options are either an expectant policy—spontaneous resolution of haematoma and hypertension has been reported after 3 weeks of injury, or an active interventional policy, with options of nephrectomy, operative liberation of haematoma or laparoscopic removal of haematoma. Longstanding haematomata can organize into fibrous pseudocapsules, or can cause irreversible renal parenchymal damage.

Because of the rarity of the disease and lack of controlled trials, no clear recommendations can be followed and therapy of Page kidney will be individualized for each case bearing in mind the condition of the patient, and the estimated time the kidney was compressed. In our three cases, single functional kidneys were involved which meant acute renal failure, which precluded an expectant approach and mandated surgical intervention. There was a successful outcome in terms of blood pressure control and renal function in all three cases following active surgical exploration and haematoma-evacuation.

Conflict of interest statement. None declared.



   References
 Top
 Introduction
 Case 1
 Case 2
 Case 3
 Discussion
 References
 

  1. Graves JW. Management of difficult to control hypertension. Mayo Clin Proc 2000; 75: 278–284
  2. Anderson GH, Blakeman N, Streeten DHP. The effect of age on prevalence of secondary forms of hypertension in 4429 consecutively referred patients. J Hypertens 1994; 12: 609–615[ISI][Medline]
  3. Page IH. The production of persistent arterial hypertension by cellophane perinephritis. J Am Med Assoc 1939; 113: 2046–2048
  4. Engel WJ, Page IH. Hypertension due to renal compression resulting from subcapsular hematoma. J Urol 1955; 73: 735–739[Medline]
  5. Aragona F, Artibani W, Calabro A et al. Page kidney: a curable form of arterial hypertension. Case report and review of the literature. Urol Int 1991; 46: 203–207[ISI][Medline]
  6. Bongu S, Faubert PF, Porush JG et al. Uncontrolled hypertension and hyperreninemia after hemorrhage in a patient with end-stage renal disease and acquired renal cysts. J Am Soc Nephrol 1994; 5: 22–26[Abstract]
  7. Cromie WJ, Jordan MH, Leapman SB. Pseudorejection: the Page kidney phenomenon in renal allografts. J Urol 1976; 116: 658–659[ISI][Medline]
  8. Juma S. Spontaneous subcapsular hematoma in an ectopic kidney. Urology 1990; 35: 448–449[ISI][Medline]
  9. Nguyen BD, Nghiem DD, Adatepe MH. Page kidney phenomenon in allograft transplant. Clin Nuclear Med 1994; 19: 361–363[ISI][Medline]
  10. Chamorro HA, Forbes TW, Padkowsky GO, Wholey MH. Multiimaging approach in the diagnosis of Page kidney. Am J Roentgenol 1981; 136: 620–633[ISI][Medline]
Received for publication: 18. 2.03
Accepted in revised form: 18. 4.03





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