Page Kidney

Article Author:
Prabhakar Vaidya
Article Editor:
Nancy Finnigan
Updated:
3/13/2019 6:25:10 PM
PubMed Link:
Page Kidney

Introduction

Page kidney or Page phenomenon results from external compression of the kidney and is a rare, treatable cause of secondary hypertension that is mediated by activation of the renin-angiotensin-aldosterone system (RAAS).[1]

Etiology

The kidneys are surrounded by a smooth, tough fibrous capsule which has limited space and a small amount of fluid under the capsule can cause compression of the kidney parenchyma resulting in Page kidney. Gerota’s fascia, on the other hand, is a larger space and can accommodate a considerable amount of blood or fluid before kidney parenchyma is compressed. In most cases of Page kidney, the compression causing hypertension is extracapsular.

External compression of the kidney may be due to a collection of blood or from some other source. Bleeding around the kidney may result from blunt trauma (sports injuries like football, hockey, other contact sports, motor vehicle accident, violence or fall), may be iatrogenic (following biopsy of native or transplant kidney, extracorporeal shockwave lithotripsy, ureteral surgery, sympathetic nerve block), or may be spontaneous (anticoagulation, AV malformation, tumor, vasculitis, pancreatitis). Non-bleeding causes of external compression include lymphoceles particularly around the transplanted kidney, urinoma, retroperitoneal paraganglioma, or large simple cysts.[1][2]

Epidemiology

In the older literature, the typical patient was a young, healthy male athlete who presented with hypertension and who had a sports-related injury in the past. In recent years, the majority of cases are iatrogenic and related to procedures or operations done on or around kidneys and reported to occur at all ages.

Pathophysiology

Irvin Page first described this entity in 1939. He performed animal experiments in which he wrapped the kidneys in cellophane. An intense inflammatory response followed and produced a fibrocollagenous shell that compressed the kidney. Compression of intrarenal vessels leads to ischemia and activation of RAAS. Hypertension developed within 4 to 5 weeks and was cured by nephrectomy of the affected kidney.[1][3]

In 1955, Engels and Page described the first case of Page kidney in a 19-year-young football player with a 2-year history of hypertension who had sustained flank trauma two years earlier and who was found to have a subcapsular hematoma. Hypertension was cured after nephrectomy.

Hypertension in Page kidney is mediated by activation of RAAS and mechanism of hypertension is similar to Goldblatt hypertension. Goldblatt, in his experiments, applied clamps to the main renal artery to reduce blood flow. Hypoperfusion of the kidneys leads to the release of renin, activation of RAAS which led to hypertension. In Page kidney, external compression of the kidney leads to decreased perfusion in intrarenal blood vessels. Resultant microvascular ischemia causes activation of RAAS leading to hypertension.[2]

Proof of RAAS dependence of hypertension in this entity is suggested by finding of elevated plasma renin activity, elevated renin level in the venous effluent from the affected kidney, response of BP to Saralasin infusion or administration of RAAS blockers and normalization of BP following nephrectomy of the affected kidney.

History and Physical

Hypertension is the main manifestation of Page kidney and may develop rapidly after the causative event or may be slow in onset and occur a long time after the causative event. The history of trauma may not be obvious. In cases of recent perinephric bleeding, a flank hematoma may be seen. Otherwise, there are no significant abnormalities on physical examination in patients with Page kidney except for hypertension. Renal function is typically normal if compression of the kidney is unilateral since the contralateral normal kidney can compensate. Renal function may be impaired if the external renal compression is bilateral or there is compression of a single functioning kidney, e.g., transplant kidney.

Evaluation

Page kidney is most often diagnosed based upon imaging studies. Ultrasonography and computed tomography of the kidneys are the most frequently used modalities. Ultrasound has the advantage of being cheap, quick, easy to perform, easily available, and noninvasive. However, it can miss small subcapsular hematoma. CT scan of the abdomen has similar advantages and has the benefit of being able to detect small hematomas and is most frequently used.[4][5]

Renal vein renin determination can certainly prove activation of RAAS as the causative mechanism of hypertension but is frequently not done.

Treatment / Management

Activation of RAAS mediates hypertension in this condition, and hence the ideal agents for the treatment of hypertension are RAAS blockers.[3] Medical treatment of hypertension may be required for short period if the cause of renal compression resolves spontaneously or following intervention, e.g., resorption or evacuation of subcapsular hematoma. Intervention may be needed for larger, symptomatic or enlarging collections or those with poorly controlled hypertension. This may require open or percutaneous drainage of the compressing collection. If the collection has been of long standing, a fibrocollagenous shell may have formed, and this may require decapsulation of this shell or even nephrectomy. Elevation of blood pressure is permanent in some cases, and lifelong antihypertensive drug therapy may be needed.[6][7]

Differential Diagnosis

If the history of flank trauma is not available and the patient presents with hypertension, it would be impossible to diagnose Page kidney because there are no unique physical findings to suggest the disease. Imaging is the way to identify the disease. Elevated renin level indicates RAAS activation as the cause of hypertension and may be due to renal artery stenosis, juxtaglomerular cell tumor, malignant hypertension.

Pearls and Other Issues

Page kidney or Page phenomenon results from external compression of the kidney and is a rare, treatable cause of secondary hypertension which is mediated by activation of the renin-angiotensin-aldosterone system (RAAS). External compression of the kidney may be due to a collection of blood or from some other source. Bleeding around the kidney may result from blunt trauma (sports injuries like football, hockey, other contact sports, motor vehicle accident, violence or fall), may be iatrogenic (following biopsy of native or transplant kidney, extracorporeal shockwave lithotripsy, ureteral surgery, sympathetic nerve block) or may be spontaneous (anticoagulation, AV malformation, tumor, vasculitis, pancreatitis). Non-bleeding causes of external compression include lymphoceles particularly around the transplanted kidney, urinoma, retroperitoneal paraganglioma or large simple cysts. Diagnosis is based on imaging studies, either abdominal ultrasound or computed tomography of the abdomen. Activation of RAAS mediates hypertension in this condition, and hence the ideal agents for the treatment of hypertension are RAAS blockers, pen or percutaneous drainage of the compressing collection. If the collection has been of long standing, a fibrocollagenous shell may have formed, and this may require decapsulation of this shell or even nephrectomy.[8][9][10]

Enhancing Healthcare Team Outcomes

Page kidney is a rare but potentially treatable and curable form of hyperension and requires awareness of the entity by primary care providers, nephrologists and other providers and a close coordination of care with radiologists in making the diagnosis and urologists in providing urologial options like percutaneous draiage or capsulectomy which may result in improvment in control or cure of hypertension.[2][6][8](Level 5)


References

[1] Haydar A,Bakri RS,Prime M,Goldsmith DJ, Page kidney--a review of the literature. Journal of nephrology. 2003 May-Jun;     [PubMed PMID: 12832730]
[2] Dopson SJ,Jayakumar S,Velez JC, Page kidney as a rare cause of hypertension: case report and review of the literature. American journal of kidney diseases : the official journal of the National Kidney Foundation. 2009 Aug;     [PubMed PMID: 19167799]
[3] Wahdat R,Schwartz C,Espinosa J,Lucerna A, Page kidney: taking a page from history. The American journal of emergency medicine. 2017 Jan;     [PubMed PMID: 27439385]
[4] Arslan S, Bilateral nontraumatic recurrent Page kidney. Radiology case reports. 2017 Sep;     [PubMed PMID: 28828114]
[5] Kiczek M,Udayasankar U, Page Kidney. The Journal of urology. 2015 Oct;     [PubMed PMID: 26173105]
[6] Smyth A,Collins CS,Thorsteinsdottir B,Madsen BE,Oliveira GH,Kane G,Garovic VD, Page kidney: etiology, renal function outcomes and risk for future hypertension. Journal of clinical hypertension (Greenwich, Conn.). 2012 Apr;     [PubMed PMID: 22458742]
[7] Whitworth PW 3rd,Dyer RB, The     [PubMed PMID: 28393300]
[8] Davies MC,Perry MJ, Urological management of 'page kidney'. BJU international. 2006 Nov;     [PubMed PMID: 17034594]
[9] Castle EP,Herrell SD, Laparoscopic management of page kidney. The Journal of urology. 2002 Aug;     [PubMed PMID: 12131346]
[10] Moriarty KP,Lipkowitz GS,Germain MJ, Capsulectomy: a cure for the page kidney. Journal of pediatric surgery. 1997 Jun;     [PubMed PMID: 9200080]