Epidemiology
Etiology
Pathophysiology
- Narrowing of one or both renal arteries → obstruction of renal blood flow → ischemia → renin release and activation of the renin-angiotensin-aldosterone system → hyperreninemic hyperaldosteronism (increased renin → increased angiotensin → increased aldosterone) → increased sodium retention and peripheral vascular resistance → renovascular hypertension (secondary hypertension)
- Prolonged renal hypoperfusion → chronic stimulation of the juxtaglomerular apparatus to secrete renin → hyperplasia of the juxtaglomerular apparatus
- No improvement in renal blood flow → ischemic renal injury → renal insufficiency and progressive renal atrophy (unilateral or bilateral depending on laterality of RAS)
Clinical features
- Family history of hypertension is often absent.
- Hypertension: severe (i.e., resistant to therapy) and/or early-onset (i.e, hypertension in individuals < 30 years of age)
- Abdominal bruit heard over the flank or epigastrium: present during both systole and diastole
- Flash pulmonary edema
- Features of atherosclerosis in other parts of the body (e.g., peripheral artery disease, coronary artery disease, carotid stenosis)
Diagnostics
- New-onset or worsening of renal dysfunction (↑ serum creatinine) after initiating ACE inhibitors or ARBs
- ACE inhibitors and ARBs can induce or worsen renal insufficiency, particularly in patients with severe bilateral renal artery stenosis or high-grade unilateral stenosis.
- Unexplained renal atrophy or asymmetry of > 1.5 cm between the kidneys
- Unexplained acute pulmonary edema
- DDx: Fibromuscular dysplasia
Treatment