Renal Artery Stenosis & Hypertension

Hypertension, commonly known as the silent killer, casts its shadow over more than 30-35% of the urban population. Within this realm, renovascular hypertension emerges as a significant subtype demanding a specialized approach due to it potential complications. Renovascular hypertension, at its core, is systemic hypertension resulting from compromised blood supply to the kidneys, typically attributed to an occlusive lesion in the main renal artery. The gravity of this condition is underscored by its association with resistant hypertension, often becoming the underlying etiology in 75% of secondary hypertension cases.

The primary culprit behind renovascular hypertension is renal artery stenosis secondary to atherosclerosis, predominantly observed in the elderly. In contrast, fibromuscular dysplasia, a condition more prevalent in young females, accounts for approximately 10% of renovascular hypertension and 5.8% of secondary hypertension. Other contributors to this hypertensive state include arteritides such as Takayasu’s, antiphospholipid antibody, extrinsic compression of the renal artery, radiation fibrosis, among others.

The historical narrative of a patient can unveil crucial indicators pointing towards renovascular hypertension. These include a history of resistant hypertension, the trial of multiple medications to control blood pressure, recurrent admissions for hypertensive care, a significant elevation in creatinine after initiating angiotensin-converting enzyme inhibitors, the presence of other atherosclerotic diseases in older individuals, etc.

Complications arising from renovascular hypertension are diverse and severe, spanning renal failure, myocardial infarction, stroke, pulmonary edema, retinopathy, aneurysm formation etc. The diagnostic journey for this condition involves a battery of laboratory tests, including urine analysis, blood urea, serum creatinine, basal metabolic profile, complement levels, autoimmune profile, plasma free metanephrine, 24-hour urinary fractionated metanephrines or normetanephrines, plasma renin-aldosterone ratio, and 24-hour urinary free cortisol.

Imaging tests play a crucial role, encompassing duplex ultrasonography, CT angiography, magnetic resonance angiography (MRA), nuclear medicine ACE-inhibitor renography, and catheter angiography, with the latter currently regarded as the gold standard for evaluating renovascular hypertension due to its superior temporal and spatial resolution.

In terms of management, the American College of Cardiology and the American Heart Association (ACC/AHA) advocate pharmacological therapy as the primary line of treatment for renal artery stenosis. Angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin II receptor blockers (ARBs) stand as cornerstones in managing renovascular hypertension. Complementary agents such as calcium channel blockers (CCBs), thiazides, beta-blockers, and hydralazine have demonstrated efficacy in controlling blood pressure for patients with renal artery stenosis. For those requiring invasive intervention, percutaneous angioplasty emerges as the treatment of choice for renovascular hypertension due to fibromuscular dysplasia and for patients with atherosclerotic renal artery stenosis not adequately controlled with medications.

The guidelines provided by the ACC/AHA underscore the recommendation for surgery in specific scenarios. These include cases of renal artery stenosis secondary to fibromuscular dysplasia, particularly those with complex disease or microaneurysms, atherosclerotic renal artery stenosis involving multiple vessels or the primary branch of the main renal artery, and atherosclerotic renal artery stenosis necessitating pararenal aortic reconstruction.

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