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Renal Artery Stenosis for the USMLE Step 1 Exam
  • Definition:
    • Renal artery stenosis (RAS) is the narrowing of one or both renal arteries, leading to decreased blood flow to the kidneys. This results in secondary hypertension due to activation of the renin-angiotensin-aldosterone system (RAAS) and can lead to chronic kidney disease if untreated.
  • Etiology:
    • Atherosclerosis:
    • The most common cause of RAS, typically seen in older adults with cardiovascular risk factors such as hypertension, diabetes mellitus, and hyperlipidemia. Atherosclerotic plaques form in the proximal renal artery, causing gradual narrowing and decreased perfusion.
    • Fibromuscular Dysplasia (FMD):
    • A less common cause of RAS, often seen in younger women. FMD is characterized by abnormal growth within the artery wall, leading to areas of stenosis alternating with areas of aneurysmal dilation, producing a “string of beads” appearance on angiography.
    • Other Causes:
    • Include vasculitis (e.g., Takayasu arteritis), external compression by tumors, or congenital abnormalities.
  • Pathophysiology:
    • Decreased Renal Perfusion:
    • Narrowing of the renal arteries reduces blood flow to the kidneys, which the body interprets as hypotension. This activates the RAAS, leading to increased production of renin, angiotensin II, and aldosterone. The result is systemic vasoconstriction, sodium retention, and water retention, ultimately causing hypertension.
    • Hypertensive Mechanism:
    • In unilateral RAS, the unaffected kidney compensates by excreting excess sodium and water, but in bilateral RAS or in patients with a solitary functioning kidney, this compensation is inadequate, leading to volume overload and resistant hypertension.
    • Ischemic Nephropathy:
    • Chronic reduction in renal blood flow can lead to kidney damage and ischemic nephropathy, causing progressive renal atrophy and, ultimately, chronic kidney disease (CKD).
Renal artery stenosis - pathophysiology
  • Clinical Features:
    • Hypertension:
    • Most commonly, RAS presents as secondary hypertension, often resistant to antihypertensive medications. Hypertension may be of recent onset in older adults or sudden worsening in patients with previously controlled blood pressure.
    • Renal Dysfunction:
    • Decreased renal perfusion in bilateral RAS or a solitary kidney can lead to a gradual decline in kidney function, presenting as chronic kidney disease or acute kidney injury. A sharp rise in serum creatinine after starting an ACE inhibitor or ARB is suggestive of bilateral RAS.
    • Abdominal Bruit:
    • A systolic-diastolic bruit may be auscultated over the abdomen, although this is not always present.
  • Diagnosis:
    • Clinical Suspicion:
    • RAS should be considered in patients with resistant hypertension, unexplained worsening of renal function, or recurrent episodes of flash pulmonary edema.
    • Imaging:
    • Duplex Ultrasound: A non-invasive screening tool that detects increased blood flow velocity in the renal arteries, suggesting stenosis.
    • CT Angiography (CTA): Provides detailed images of the renal vasculature but requires contrast, limiting its use in patients with renal dysfunction.
    • Magnetic Resonance Angiography (MRA): Useful for patients with chronic kidney disease; however, gadolinium-based contrast should be avoided in severe kidney disease due to the risk of nephrogenic systemic fibrosis.
    • Renal Arteriography: The gold standard for diagnosis, providing direct visualization of the stenosis and allowing for therapeutic intervention (angioplasty).
  • Management:
    • Medical Therapy:
    • Antihypertensive Medications: ACE inhibitors or ARBs are first-line agents but should be used with caution in bilateral RAS or a solitary kidney due to the risk of acute kidney injury. Diuretics and calcium channel blockers may also be used for blood pressure control.
    • Statins: Indicated for patients with atherosclerotic RAS to reduce cardiovascular risk.
    • Revascularization:
    • Percutaneous Transluminal Angioplasty (PTA): May be indicated in patients with fibromuscular dysplasia or atherosclerotic RAS with resistant hypertension, worsening renal function, or recurrent pulmonary edema. PTA can be performed with or without stenting.
    • Surgical Revascularization: Rarely performed but may be considered in complex cases or when angioplasty is not feasible.
Key Points
  • Renal artery stenosis is caused primarily by atherosclerosis and fibromuscular dysplasia, leading to hypertension and renal dysfunction.
  • Clinical features include resistant hypertension, renal dysfunction, and, in some cases, an abdominal bruit.
  • Diagnosis involves imaging such as duplex ultrasound, CTA, MRA, or renal arteriography (gold standard).
  • Management includes medical therapy with antihypertensive agents and revascularization in selected patients with severe disease.

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