Renovascular Hypertension: Clinical Features, Differential Diagnoses and Basic Principles of Treatment

Abstract

Renovascular hypertension is caused by renal artery stenosis. Its prevalence in populations of hypertensive patients is 1-8%, and in populations of patients with resistant hypertension, it is up to 20%. The two main causes of stenosis are atherosclerosis and fibromuscular dysplasia of the renal artery. The main clinical consequences of renal artery stenosis include renovascular hypertension, ischemic nephropathy and “flash” acute pulmonary oedema. Unilateral stenosis of the renal artery causes angiotensin II-dependent hypertension, and bilateral stenosis of the renal arteries produces volume-dependent hypertension. Renovascular aetiology of hypertension should be questioned in patients with resistant hypertension, hypertension with a murmur identified upon auscultation of the renal arteries, and a noticeable side-to-side difference in kidney size. Non-invasive diagnostic tests include the determination of concentrations of peripheral vein plasma renin activity, the captopril test, captopril scintigraphy, colour Doppler ultrasonography, computed tomography angiography, and nuclear resonance angiography. Renovasography represents the gold standard for the diagnosis of renovascular hypertension. The indications for revascularization of the renal artery include haemodynamically significant renal artery stenosis (with a systolic pressure gradient at the site of stenosis of - ΔP ≥ 20 mmHg, along with the ratio of the pressure in the distal part of the renal artery (Pd) and aortic pressure (Pa) less than 0.9 (Pd/Pa < 0.9)), resistant hypertension, loss of renal function after administration of ACE inhibitors or angiotensin receptor II blockers, and recurrent flash pulmonary oedema associated with bilateral renal artery stenosis. The contraindications for renal artery revascularization include a longitudinal diameter of the affected kidney that is less than 8.0 cm, the resistance index measured from the segmental arteries peak blood flow (RI) > 0.8, chronic kidney disease (GFR <30 ml/min/1.73 m2) and negative captopril scintigraphy (lack of lateralization).