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Question:

A 66-year-old man comes to the clinic for a follow-up for hypertension.  Two months ago during a routine office visit, his blood pressure was 165/95 mm Hg.  The patient has since had 2 follow-up visits, both documenting high blood pressure.  The patient states that he currently has no symptoms and has never been diagnosed with hypertension, but he does have type 2 diabetes mellitus and hyperlipidemia.  He underwent a stent placement for peripheral vascular disease 2 years ago.  The patient is a former cigarette smoker with a 25-pack-year history.  Currently, his blood pressure is 162/93 mm Hg, and his pulse is 73/min and regular.  BMI is 31 kg/m2.  Physical examination is unremarkable.  Serum creatinine is 0.8 mg/dL.  CT angiography reveals 80% atherosclerotic narrowing of the right renal artery.  In addition to antihyperlipidemic therapy, which of the following is the best next step in management of this patient?

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Explanation:

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Renal artery stenosis (RAS) is most often seen in patients with diffuse atherosclerosis (eg, peripheral vascular disease) and results in renovascular hypertension, the most common, correctable cause of secondary hypertension.  Limited blood flow to the poststenotic kidney leads to activation of the renin-angiotensin-aldosterone system.  Although this helps increase renal blood flow (RBF) to the stenotic kidney and improves the affected kidney's glomerular filtration rate (by constricting the efferent arteriole), it is maladaptive and results in sodium retention, volume expansion, vasoconstriction, and hypertension.

ACE inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) are indicated as first-line therapy in RAS due to their ability to reduce angiotensin II levels, which improves systemic blood pressure and dilates the glomerular efferent arterioles.  ACEIs and ARBs have long-term nephroprotective effects, largely due to decreased intraglomerular pressures; studies have demonstrated that patients with RAS on ACEIs were less likely to develop myocardial infarction, stroke, or end-stage renal disease than those on other medical therapy.  However, there is a higher risk of acute kidney injury; therefore, renal function should be monitored closely.

  • In unilateral RAS, the stenotic kidney experiences reduced RBF and a fall in glomerular filtration rate (GFR), but the unaffected kidney compensates for this because it is no longer subject to angiotensin II–induced renal vasoconstriction.  The acute change in GFR is usually small. 
  • In bilateral RAS, reduction in blood flow can lead to a more significant reduction in GFR; however, most patients tolerate the medication with only a mild rise in serum creatinine. The medication may be continued if the rise remains acceptable (ie, <30%).

Additional measures should include aggressive risk factor reduction (eg, aspirin, diabetes and hyperlipidemia control, smoking cessation) to prevent cardiovascular disease.

(Choices A and C)  Several antihypertensive agents are used in conjunction with ACEIs or ARBs for adequate blood pressure control.  These include calcium channel blockers, thiazide diuretics, beta blockers, and mineralocorticoid receptor antagonists.  However, loop diuretics and doxazosin are not recommended as first-line agents for hypertension.

(Choices D and E)  Revascularization (surgical or percutaneous angioplasty with stenting) has not been proven superior to medical therapy for optimal blood pressure control or reduction of cardiovascular outcomes in patients with unilateral or bilateral RAS.  It is reserved for selected patients who are intolerant or fail to achieve adequate blood pressure control with optimal medical therapy and for those with recurrent flash pulmonary edema and/or refractory heart failure due to severe hypertension.

Educational objective:
ACE inhibitors or angiotensin receptor blockers are indicated for initial therapy in patients with renovascular hypertension (due to renal artery stenosis).  Renal artery stenting or surgical revascularization is reserved for patients with resistant hypertension or recurrent flash pulmonary edema and/or refractory heart failure due to severe hypertension.