Renal Artery Stenosis for USMLE Step 2
Renal Artery Stenosis for the USMLE Step 2 Exam
- Definition:
- Renal artery stenosis (RAS) is the narrowing of the renal arteries, causing reduced renal perfusion, activation of the renin-angiotensin-aldosterone system (RAAS), and secondary hypertension. RAS can result in ischemic nephropathy and chronic kidney disease (CKD).
- Etiology:
- Atherosclerosis:
- The leading cause of RAS, seen in about 90% of cases, primarily affecting older adults with cardiovascular risk factors like hypertension, diabetes, hyperlipidemia, and smoking. Plaque buildup leads to narrowing at the proximal renal artery.
- Fibromuscular Dysplasia (FMD):
- A non-atherosclerotic cause that typically affects young women. It leads to abnormal arterial wall growth, resulting in a “string of beads” appearance on angiography. It usually involves the mid to distal segments of the renal artery.
- Other Causes:
- Less common causes include vasculitis, neurofibromatosis, and external compression by tumors.
- Pathophysiology:
- Decreased Renal Perfusion:
- The narrowing of renal arteries reduces blood flow to the kidney, which activates RAAS. This leads to systemic vasoconstriction, sodium retention, and increased blood pressure (secondary hypertension).
- Renal Ischemia:
- In bilateral RAS or in a solitary functioning kidney, prolonged ischemia leads to ischemic nephropathy, causing kidney atrophy and progressive renal dysfunction.
- Hypertension:
- In unilateral RAS, the unaffected kidney compensates, but in bilateral RAS, the reduced perfusion drives persistent activation of RAAS, leading to uncontrolled hypertension and volume overload.
- Clinical Features:
- Resistant Hypertension:
- RAS often presents as resistant hypertension (hypertension unresponsive to ≥3 antihypertensive medications). It can also present as new-onset hypertension in older adults or abrupt worsening of preexisting hypertension.
- Renal Dysfunction:
- Bilateral RAS or RAS in a solitary kidney can lead to acute or chronic kidney injury. A marked rise in serum creatinine after initiation of an ACE inhibitor or ARB suggests RAS.
- Abdominal Bruit:
- A systolic-diastolic bruit may be heard over the epigastrium or flanks, though this is not always present.
- Flash Pulmonary Edema:
- Sudden episodes of pulmonary edema can occur in bilateral RAS or in a solitary functioning kidney, often related to volume overload.
- Diagnosis:
- Clinical Suspicion:
- RAS should be considered in cases of resistant hypertension, unexplained decline in renal function, or recurrent flash pulmonary edema.
- Imaging:
- Duplex Ultrasound: Measures blood flow velocity in the renal arteries, with elevated velocities indicating stenosis. Non-invasive and often used for screening.
- CT Angiography (CTA): Provides detailed images of the renal arteries and can identify the extent of stenosis, but requires contrast.
- Magnetic Resonance Angiography (MRA): A non-invasive option for patients with renal insufficiency, though gadolinium use may be restricted in severe CKD.
- Renal Arteriography: The gold standard for diagnosis, allowing direct visualization of stenosis and the possibility of therapeutic intervention (angioplasty).
- Management:
- Medical Therapy:
- Antihypertensive Treatment: ACE inhibitors or ARBs are first-line agents, but must be used cautiously in bilateral RAS due to the risk of renal function decline. Diuretics and calcium channel blockers are also used.
- Lipid-Lowering Therapy: Statins are indicated to manage atherosclerotic disease and reduce cardiovascular risk.
- Revascularization:
- Percutaneous Transluminal Angioplasty (PTA): Indicated for patients with fibromuscular dysplasia or severe atherosclerotic RAS with renal dysfunction or recurrent pulmonary edema.
- Surgical Revascularization: Rarely performed but may be considered in complex cases where angioplasty is not feasible.
Key Points
- Renal artery stenosis is primarily caused by atherosclerosis in older adults and fibromuscular dysplasia in younger women.
- Common clinical features include resistant hypertension, renal dysfunction, and sometimes flash pulmonary edema.
- Diagnosis is confirmed using imaging modalities such as duplex ultrasound, CT angiography, or renal arteriography.
- Management includes antihypertensive medications and revascularization (angioplasty or surgery) for severe or symptomatic cases.