Patient with bilateral renal artery bruits and hypertension will for sure have activation of RAS system and therefore increase in angiotensin.

Although pheochromocytoma and consequent elevated catecholamines can increase blood pressure, symptoms are typically episodic and renal bruits are not likely to be heard. Elevated levels of serotonin can also cause hypertension, but we would also expect to see flushing; also, there is nothing in the stem to indicate patient is taking SSRIs or something else that could predispose her to elevated levels of serotonin. Elevated levels of thyroid hormone could also give patient hypertension, but we would also expect other signs of hyperthyroidism (tremors, weight loss, etc.).

I was a little confused if EPO would be elevated -- if there is stenosis of renal arteries (as indicated by the bruits) the kidneys could also detect this as hypoxia and ramp up production of EPO. However, I ended up going with angiotensin since it seemed more "concrete" to me that RAS would be up. Does anyone know why it's not EPO?

main points from this question:

• bilateral renal bruits in a patient with HTN = Renal artery stenosis --> in a young woman, it's most likely Fibromuscular dysplasia

• RAS can present in up to 1/3 of patients with malignant HTN or hypertensive emergency which is how this patient is presenting, evidenced by the HA, blurred vision, and papilledema.

• renal artery stenosis → decreased renal perfusion → compensatory activation of the renin–angiotensin–aldosterone system → secondary hypertension