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Renal Artery Stenosis for the USMLE Step 3 Exam
  • Definition:
    • Renal artery stenosis (RAS) is the narrowing of the renal arteries, leading to reduced blood flow to the kidneys. This triggers the renin-angiotensin-aldosterone system (RAAS), causing secondary hypertension and potentially leading to renal ischemia and chronic kidney disease (CKD).
  • Etiology:
    • Atherosclerosis:
    • The most common cause, accounting for 90% of cases, typically affecting older adults with cardiovascular risk factors such as hypertension, diabetes, hyperlipidemia, and smoking. Plaques form at the origin or proximal renal artery, causing narrowing.
    • Fibromuscular Dysplasia (FMD):
    • A non-atherosclerotic cause, seen more frequently in women under 50. FMD is characterized by abnormal arterial wall growth, leading to the characteristic “string of beads” appearance on angiography. FMD usually affects the mid to distal portion of the renal artery.
    • Other Causes:
    • Vasculitis, neurofibromatosis, and external compression by tumors are rare causes of RAS.
  • Pathophysiology:
    • Decreased Renal Perfusion:
    • Narrowing of the renal arteries leads to decreased blood flow to the kidneys. This activates the RAAS, which increases renin release, leading to systemic vasoconstriction, sodium retention, and increased blood pressure.
    • Renal Ischemia:
    • Chronic ischemia due to severe or bilateral RAS leads to kidney atrophy, ischemic nephropathy, and progressive loss of renal function, ultimately resulting in CKD or end-stage renal disease (ESRD).
    • Hypertension:
    • Unilateral RAS may lead to secondary hypertension due to RAAS activation. In bilateral RAS, the lack of compensatory excretion from a healthy kidney causes volume overload and persistent hypertension.
Renal artery stenosis - pathophysiology
  • Clinical Features:
    • Resistant Hypertension:
    • A key feature, characterized by hypertension that is unresponsive to ≥3 antihypertensive medications, or new-onset hypertension in older adults. Patients may have worsening hypertension despite previous control.
    • Renal Dysfunction:
    • A rapid rise in serum creatinine following initiation of ACE inhibitors or ARBs suggests bilateral RAS or RAS in a solitary kidney. Chronic kidney disease or acute kidney injury may develop in severe cases.
    • Abdominal Bruit:
    • A systolic-diastolic bruit may be heard over the abdomen or flanks, although this is not always present.
    • Flash Pulmonary Edema:
    • Sudden episodes of pulmonary edema, often linked to fluid overload, can occur in severe or bilateral RAS, especially with a solitary kidney.
  • Diagnosis:
    • Clinical Suspicion:
    • RAS is suspected in patients with resistant hypertension, unexplained renal function decline, or recurrent flash pulmonary edema.
    • Imaging:
    • Duplex Ultrasound: A non-invasive test that detects increased blood flow velocity, indicating stenosis. Often used for initial screening.
    • CT Angiography (CTA): Provides detailed images of the renal arteries, but requires contrast, limiting its use in patients with renal dysfunction.
    • Magnetic Resonance Angiography (MRA): An alternative to CTA for patients with kidney disease, though gadolinium is avoided in advanced renal failure.
    • Renal Arteriography: The gold standard for diagnosis, allowing direct visualization of stenosis and enabling interventional procedures such as angioplasty.
  • Management:
    • Medical Therapy:
    • Antihypertensive Medications: ACE inhibitors or ARBs are first-line agents, though used cautiously in bilateral RAS due to the risk of worsening renal function. Calcium channel blockers and diuretics are often added to control blood pressure.
    • Statins and Antiplatelet Therapy: Indicated for patients with atherosclerotic RAS to reduce cardiovascular risk.
    • Revascularization:
    • Percutaneous Transluminal Angioplasty (PTA): Indicated for patients with fibromuscular dysplasia or atherosclerotic RAS with declining renal function, resistant hypertension, or flash pulmonary edema. Stenting may be required in some cases.
    • Surgical Revascularization: Reserved for complex cases where angioplasty is not feasible.
Key Points
  • Renal artery stenosis is commonly caused by atherosclerosis or fibromuscular dysplasia, leading to resistant hypertension and renal dysfunction.
  • Clinical features include resistant hypertension, renal dysfunction, and sometimes flash pulmonary edema.
  • Diagnosis is confirmed through imaging, with duplex ultrasound, CTA, and MRA being common modalities, and renal arteriography as the gold standard.
  • Management includes blood pressure control, revascularization through angioplasty, and careful monitoring of renal function in severe cases.

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