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
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