Case Presentation: A 47-year-old female with a history of hypertension was admitted with worsening dyspnea, leg swelling, and a blood pressure of 219/147. She was nonadherent to home BP meds due to cost. Exam showed signs of fluid overload, including pitting edema and jugular venous distention. Labs revealed elevated serum creatinine (1.38 mg/dL), calcium (11.0 mg/dL), NT-proBNP (8710 pg/mL), TSH (5.26 uIU/mL), and low hemoglobin (8.1 g/dL). CT scan showed abdominal wall edema, a large pancreatic pseudocyst, possible renal pelvis thickening, and evidence of liver cirrhosis. Chest X-ray indicated pulmonary edema. She was treated in the emergency room for hypertensive emergency with home BP medications that include Losartan, Metoprolol, and Amlodipine, then admitted for further management of HTN and new onset heart failure. She did not have an adequate response to home BP medication and started to experience headaches that correlated with spikes in blood pressure. She was then started on a nitroglycerin drip and diuretics. An echocardiogram showed left ventricular ejection fraction of 40%, severe left ventricular hypertrophy, and elevated pulmonary artery pressure to 58 mmHg. The nitroglycerin drip was discontinued, then isosorbide dinitrate and hydralazine were started. Despite this, her BP remained high. A renal ultrasound revealed no renal artery stenosis but absent color flow doppler of the left kidney and abnormal left kidney tissue. Nephrology recommended interventional radiology consult to drain the pancreatic pseudocyst. This restored renal artery blood flow and her BP rapidly normalized. BP meds were adjusted due to hypotension and goal-directed therapy for heart failure was initiated.
Discussion: Secondary hypertension in middle-aged patients necessitates thorough investigation, including for hyperaldosteronism, obstructive sleep apnea, and rarer phenomena like Page kidney. Page kidney is a rare reversible etiology of resistant hypertension caused by external compression of the renal parenchyma by a perirenal process, leading to incessant activation of the renin-angiotensin-aldosterone system (RAAS) and secondary systemic hypertension. Workup in these patients should include a basic metabolic panel (BMP), urinalysis, aldosterone/renin ratio, and polysomnography. Treatment aims to normalize blood pressure, which in this case was achieved through percutaneous drainage of the pancreatic pseudocyst to alleviate compression. This case underscores the importance of thorough evaluation in patients with resistant hypertension, as there are numerous potential secondary causes, including the rare phenomenon of Page kidney. In this case, hospital medicine plays a critical role in managing complex cases of secondary hypertension with multi-organ involvement, highlighting the importance of interdisciplinary collaboration and timely interventions to optimize patient outcomes.
Conclusions: Page kidney represents an uncommon etiology of secondary hypertension, predominantly resulting from iatrogenic interventions, blunt trauma, or spontaneous occurrences. The primary clinical manifestation is hypertension, often associated with a history of renal mass or abdominal trauma. Impairment in renal function is more frequently observed in patients with a solitary functioning kidney. Prompt diagnostic evaluation and therapeutic intervention are imperative, given that the most severe complication associated with this condition is renal failure.