Write a short note on renal artery stenosis.

Definition

Renal artery stenosis (RAS) is narrowing of one or both main renal arteries or their branches, sufficient to reduce renal perfusion. It is important as a potentially correctable cause of secondary hypertension and of progressive renal impairment — "ischaemic nephropathy".

Aetiology

Pathophysiology

Reduced renal perfusion is sensed by the juxtaglomerular apparatus, activating the renin–angiotensin–aldosterone system:

• Renin → angiotensin II → vasoconstriction and aldosterone release → sodium and water retention → HYPERTENSION
• Angiotensin II maintains the efferent arteriolar tone necessary to preserve glomerular filtration in the hypoperfused kidney — which is precisely why ACE inhibitors and ARBs precipitate acute kidney injury in bilateral disease (see the danger box)
• Chronic ischaemia causes tubulointerstitial fibrosis and atrophy — ischaemic nephropathy — with progressive irreversible loss of function

Clinical Features — When to Suspect It

• Severe or resistant hypertension — uncontrolled despite three drugs including a diuretic.
• Hypertension of abrupt onset, or onset before 30 (fibromuscular dysplasia) or after 55 (atherosclerotic).
• Sudden worsening of previously controlled hypertension; malignant or accelerated hypertension.
• Deterioration in renal function after starting an ACE inhibitor or ARB — the classic clue.
• "FLASH" PULMONARY OEDEMA — recurrent, sudden pulmonary oedema with preserved left ventricular function (Pickering syndrome), characteristic of bilateral disease.
• Unexplained progressive renal impairment, particularly with a discrepancy in kidney size on ultrasound (a difference of more than 1.5 cm).
• Abdominal or flank BRUIT — systolic-diastolic, specific though insensitive.
• Widespread atherosclerotic disease elsewhere.
• Hypokalaemia with metabolic alkalosis (secondary hyperaldosteronism), and absence of proteinuria or an active sediment — which distinguishes it from intrinsic renal disease.

Investigations

Also assess: renal function, electrolytes (hypokalaemia), urinalysis (typically bland with little proteinuria), lipids, glucose, and evidence of atherosclerosis elsewhere.

Management

1. Medical therapy is the mainstay for atherosclerotic disease

This reflects a genuine change in practice: large randomised trials (ASTRAL and CORAL) showed that revascularisation added no benefit over optimal medical therapy for most patients with atherosclerotic renal artery stenosis, in terms of blood pressure, renal function or cardiovascular events.

• Blood pressure control — ACE inhibitors or ARBs are effective and appropriate in UNILATERAL disease, with careful monitoring of creatinine and potassium; combine with other agents as needed.
• Statin therapy and antiplatelet therapy.
• Smoking cessation, glycaemic control, weight and dietary sodium management.
• Monitor renal function and kidney size.

2. Revascularisation — for selected patients only

• Percutaneous angioplasty (with stenting for atherosclerotic ostial lesions; angioplasty alone is usually sufficient and highly effective for fibromuscular dysplasia).
• Indications: fibromuscular dysplasia (where results are excellent and often curative), recurrent flash pulmonary oedema, rapidly deteriorating renal function, truly refractory hypertension despite maximal medical therapy, and critical stenosis in a solitary functioning kidney.
• Surgical revascularisation — reserved for complex anatomy or failed endovascular treatment.

3. Treat the underlying condition — immunosuppression for Takayasu arteritis before considering intervention.