Renal artery stenosis and Secondary hypertension

Renal artery stenosis is the narrowing of one or both renal arteries, which leads to hypertension and renal atrophy.

Etiology

Atherosclerosis

The majority of cases (nearly 90%) are associated with lumen narrowing due to atherosclerotic plaque, which occurs more in men > 50 years of age. Atherosclerotic RAS (ARAS) typically involves the proximal third of the renal artery including the perirenal aorta and ostium. In these patients, atherosclerosis is generally systemic and not limited to the renal artery, and elderly patients present with multiple cardiovascular risk factors (hyperlipidemia, smoking, history of stroke, etc).

Fibromuscular dysplasia (FMD)

There is a thickening of the renal arterial wall causing luminal narrowing in (nearly 10% of cases). It mostly affects women < 40 years of age. FMD has classically been described as having a “beads-on-a-string” appearance due to contrast filling of consecutive aneurysms along the renal artery. In fibromuscular dysplasia, the muscle and fibrous tissues in the arterial wall thickening, causing the arteries to narrow. This may reduce blood flow to the kidney, leading to kidney damage and Renovascular hypertension.

Other causes include vasculitis, external compression, and radiation therapy.

Pathophysiology

Renal artery stenosis/luminal narrowing → reduced renal perfusion and slow pressure in renal vasculature → activation of RAAS (renin-angiotensin-aldosterone system) → Increased renin and aldosterone → Increased sodium and water reabsorption → Sodium and water retention → volume expansion → Increased peripheral vascular resistance → Renovascular hypertension (secondary hypertension).

Long-standing renal hypoperfusion → continuous stimulation of the juxtaglomerular apparatus to secrete renin → juxtaglomerular apparatus hyperplasia

Ischemic nephropathy

Severe reduction in renal blood flow → ischemia of renal tissue → renal insufficiency, cortical thinning and progressive renal atrophy →Chronic kidney disease and renal failure

Left ventricular hypertrophy and pulmonary edema

Increased Peripheral vascular resistance → increased afterload → left ventricular hypertrophy →increased left ventricular filling pressure → reduced ejection fraction → pulmonary edema

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Clinical presentation

Hypertension which doesn’t respond to usual antihypertensive medicine
Deterioration in renal function after taking an ACE inhibitor or angiotensin receptor blocking (ARB) agent
heart failure or pulmonary edema

Diagnosis

Duplex Ultrasonography
CT or MR angiography
Invasive Catheter Angiography (gold standard)

Treatment

Antihypertensive medicine

ACE-inhibitors or ARBs

Given with precautions, and regular serum creatinine level checkups
Contraindicated in B/LRenal stenosis and patient with a single kidney

Calcium channel blockers or beta-blockers in patients not responding to ACE inhibitors, or where it is contraindicated.

Surgical intervention

Revascularization

Reserved for cases which don’t respond to medical treatment

Balloon dilation of the stenosis
Stent placement

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