Causes of secondary hypertension
Condition	Clinical clues/features
Renal parenchymal disease	Elevated serum creatinine Urinalysis abnormalities (eg, proteinuria, RBC casts)
Renal artery stenosis	Systolic-diastolic abdominal bruit Recurrent flash pulmonary edema Marked AKI following initiation of ACE inhibition
Primary hyperaldosteronism	Hypokalemia (spontaneous or thiazide induced) Metabolic alkalosis
Obstructive sleep apnea	Daytime somnolence BMI >35 kg/m², large neck circumference
Pheochromocytoma	Paroxysmal hypertension & tachycardia Episodic headaches, palpitations, diaphoresis
Cushing syndrome	Cushingoid body habitus, proximal muscle weakness Hyperglycemia
Thyroid dysfunction	Hyperthyroidism: anxiety, heat intolerance, weight loss, tachycardia Hypothyroidism: fatigue, cold intolerance, weight gain, bradycardia
Primary hyperparathyroidism	Mild-to-moderate hypercalcemia ± symptoms Nephrolithiasis
Coarctation of the aorta	Headaches & epistaxis Upper extremity hypertension with brachial-femoral pulse delay
AKI = acute kidney injury; RBC = red blood cell.

This patient has elevated blood pressure despite multiple medications, consistent with resistant hypertension. Resistant hypertension is defined as persistently elevated blood pressure despite treatment with >3 antihypertensive agents of different classes (one being a diuretic). Patients with resistant hypertension and those with severe or malignant hypertension should be evaluated for secondary causes of hypertension. Patients experiencing a sudden blood-pressure rise in the setting of previously well-controlled blood pressure or with age of onset <30 and no family history of hypertension should be also evaluated for secondary hypertension.

Renovascular disease (eg, atherosclerotic renal artery stenosis) is the most common correctable cause of secondary hypertension. Features suggesting renal artery stenosis (RAS) include:

Rise in serum creatinine >30% from baseline after starting an ACE inhibitor or angiotensin receptor blocker
Severe hypertension with recurrent flash pulmonary edema
Severe hypertension in patients with diffuse atherosclerosis
Onset of severe hypertension after age 55
Hypertension in a patient with asymmetric kidney size (small atrophic unilateral kidney)
Abdominal bruit

This patient has multiple risk factors (smoking, diabetes, hyperlipidemia) and clinical evidence of diffuse atherosclerosis. RAS is present in about 1% of patients with mild hypertension. However, it has been found in up to 45% of white patients with severe hypertension and in 25%-35% of patients with peripheral arterial disease. The presence of an abdominal bruit (up to 99% specific but only 40% sensitive) is highly suggestive of RAS.

(Choice B) An elevated plasma aldosterone/renin activity ratio >20:1 is seen in patients with primary hyperaldosteronism, which is a common cause of resistant hypertension. However, the presence of diffuse atherosclerosis makes RAS the more likely cause in this patient.

(Choice C) An increased 24-hour urinary free cortisol excretion is observed in Cushing's syndrome. Cushing's syndrome can cause hypertension. However, these patients typically have additional clinical features such as central obesity, facial plethora, muscle wasting, thin skin, psychological changes, or hirsutism.

(Choice D) Urinary excretion of metanephrines is increased in pheochromocytoma. These patients generally experience symptoms (eg, episodic headaches, tachycardia, sweating) associated with paroxysmal elevations in blood pressure.

(Choice E) Aortic coarctation is associated with rib notching on chest x-ray due to enlarged collateral intercostal vessels. It usually presents with brachial-femoral pulse delay, high blood pressure in the arms compared to the lower extremities, and a continuous murmur over the back. However, it is usually diagnosed in children.

Educational objective:
Renovascular hypertension should be suspected in patients who have resistant hypertension with diffuse atherosclerosis, asymmetric kidney size, recurrent flash pulmonary edema, or acute rise in serum creatinine after starting an ACE inhibitor or angiotensin receptor blocker. A central abdominal bruit is highly specific for renovascular hypertension.

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