A 70-year-old man comes to the office due to increasing headaches, nausea, and vomiting. The patient has never had these symptoms before. Medical history is significant for a transient ischemic attack that led to a right carotid endarterectomy 5 years ago. He has no other medical conditions, and his only medications are aspirin and atorvastatin. The patient smoked a pack of cigarettes a day for 20 years but quit 20 years ago. Blood pressure is 220/120 mm Hg and pulse is 70/min. Neurologic examination shows no focal lesions. Bilateral abdominal bruits are present. Blood testing in this patient would most likely show which of the following?

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11ec160b_3c73_18c4_9249_35461dfda74b_MD0001_00 This patient has a hypertensive emergency, with markedly elevated blood pressure and symptoms (headache, vomiting) suggesting elevated intracranial pressure. In conjunction with his bilateral abdominal bruits (abnormal sound caused by turbulent blood flow), this presentation suggests renovascular hypertension from bilateral renal artery stenosis (RAS). Although RAS can be caused by a variety of lesions (eg, fibromuscular dysplasia in young women), >90% of cases are caused by atherosclerotic narrowing of the proximal renal artery. Therefore, it is most common in older patients with other atherosclerotic disease (eg, carotid stenosis, as in this patient) or risk factors (eg, diabetes, hyperlipidemia, smoking). Decreased renal artery perfusion activates the renin-angiotensin-aldosterone system. The juxtaglomerular cells increase secretion of renin, which converts angiotensinogen to angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme. Angiotensin II, a potent vasoconstrictor, causes increased peripheral resistance and elevated systemic blood pressure. In addition, it stimulates the secretion of aldosterone, which increases renal Na⁺ reabsorption and K⁺ and H⁺ excretion, resulting in relative hypokalemia and metabolic alkalosis. Educational objective: Renal artery stenosis (eg, severe hypertension, abdominal bruits) causes decreased renal artery perfusion, which activates the renin-angiotensin-aldosterone system. Increased secretion of renin leads to increased production of angiotensin I and angiotensin II, which causes increased peripheral resistance and elevated systemic blood pressure. Increased aldosterone secretion causes increased renal Na⁺ reabsorption and K⁺ and H⁺ excretion, resulting in relative hypokalemia and metabolic alkalosis.

A 70-Year-Old Man Comes to the Office Due to Increasing