Page kidney was initially described by Page in 1939 (
2). The main mechanism responsible for emergence of accelerated HTN and hypokalemia is believed to be RAAS-mediated. Although Page kidney seems to be similar to the Goldblatt model of renovascular HTN, the latter is due to compression or stenosis of major renal vessels. On the other hand, Page kidney seems to be the result of an ischemic renal vascular insult. Up to this date, approximately 110 cases are reported in literature (
3). Most cases are due to compression of the kidney by a subcapsular or perinephric hematoma. Earlier blunt abdominal trauma was the major cause of this hematoma although nowadays many cases (ten out of 28 cases) are iatrogenic injuries following renal transplant biopsy of the kidney (
4). In our case, the reason behind hypotension was bleeding from splenic artery aneurysm, which evolved as a complication to chronic pancreatitis, while the development of accelerated HTN was due to the perinephric hematoma. However, the case we reported here is the first of its kind. Up to this date, no case of Page kidney consequent to splenic artery aneurysm has been reported. Pathological Page kidney is seen in acute and chronic types. The acute type is due to the collection of blood or fluid in the subcapsular or perinephric space, which is often short lived, and the chronic type has a delayed onset and is caused by a fibrocollagenous scar compressing the renal parenchyma. Renal insufficiency is not usually seen because of normal perfusion of contralateral kidney, which maintains normal renal function. With time, renal function may gradually decline due to progressive shrinkage of the affected kidney. The development of HTN and deterioration of the renal function probably occurs due to the compression-induced interstitial nephritis. However, in cases of renal allograft or solitary kidney, renal insufficiency may need urgent surgical intervention. Page kidney can be diagnosed by multiple imaging techniques with each modality having its own advantages and disadvantages. Ultrasound is easily available, cheap, and noninvasive; however, small perinephric hematomas can be missed due to its high operator dependence. By assessing the vascularity, color Doppler ultrasound can be helpful not only in diagnosing Page kidney but also in excluding renal artery stenosis. Abdominal CECT is noninvasive and has high sensitivity and specificity in diagnosis of very small hematomas; hence, it has become the modality of choice. Magnetic resonance angiography is helpful in evaluating the age of hematomas and patency of renal vessels. Other investigations such as intravenous urography (IVU), nuclear scan, and renal arteriography also play a role in diagnosing perinephric hematoma.
The initial treatment usually involves drugs such as angiotensin convertase enzyme inhibitors (ACEIs) or aldosterone receptor blocker (ARB) with the aim of normalizing high blood pressure. The inability of a single agent to control the blood pressure necessitates the combination of multiple drugs such as beta blockers and calcium channel blockers (
5). Earlier definitive treatment of Page kidney involved radical nephrectomy or open surgery to evacuate the hematoma or performing a decapsulating procedure to save the normal kidney (
6,
7). The current approach is inclined toward less invasive procedures such as angioembolization and percutaneous drainage.
To summarize, Page kidney is a rare cause of HTN secondary to RAAS activation. Although splenic artery aneurysm due to chronic pancreatitis is a very uncommon cause of Page kidney, early evaluation by CECT of abdomen and renal angiogram are diagnostic and less invasive procedures such as angioembolization and percutaneous drainage promise favorable outcome.