An Unusual Case of Renovascular Hypertension in a Pediatric Patient Associated with Hyponatremia and Polyuria Responding to Angioplasty and Losartan

Introduction: Renovascular abnormalities are an important cause of secondary hypertension in pediatric population. Hyponatremia and polyuria are uncommon complications. Case Description: This is a report of a 13-year-old female who developed hypertensive emergency secondary to unilateral renal artery stenosis. She presented with a two-week history of severe headaches, nausea, vomiting, polyuria and enuresis. Initial Blood Pressure (BP) was 196/132mmHg. It was safely lowered over 48 hours to 115-130mmHg range using Nicardipine infusion. Laboratory tests on admission showed Sodium 128 mmol/L, Potassium 2.1 mmol/L, Plasma Renin Activity (220ng/ml/hr, normal limit<2.4), and Aldosterone levels (45ng/dL,normal<21). Echocardiography revealed mild concentric left ventricular hypertrophy, with normal aorta. Computerized Tomography Angiography (CTA) showed delayed enhancement of the relatively small size right kidney with stenosis of the ostium of its main artery. Digital Subtraction Angiography done on hospital day #5, confirmed CTA findings and demonstrated presence of collateral flow through a hypertrophied right adrenal artery which explains kidney viability despite severe stenosis. Balloon angioplasty was successful in restoring blood flow with 15-20% residual stenosis. Post-procedure, she required less Nicardipine infusion and subsequently transitioned to oral Amlodipine. Polyuria and hyponatremia were observed upon admission and persisted despite achieving BP target early during hospitalization, after angioplasty it started to improve. Losartan 12.5mg was commenced on day 7 with further improvement in polyuria and no further need for salt supplementation (figure 1 and 2). Discussion: Renovascular disease can lead to life threatening hypertensive emergencies. Excessive diuresis and hyponatremia have complicated the management of our case. It required efforts to replace losses using large volumes of fluids and sodium chloride to maintain homeostasis. Hyperfiltration due to Angiotensin II excess is the plausible underlying mechanism; this explains why It started to improve gradually following angioplasty and the addition of Losartan.