Treatment options for renovascular hypertension.
Renovascular hypertension is usually caused by atherosclerotic narrowing of the origin of the renal artery and is much more common than is thought among patients with peripheral vascular disease, carotid stenosis or heart failure. Renovascular hypertension must be distinguished from renal artery stenosis. In true renovascular hypertension, the kidney takes charge of the blood pressure and will do what it takes to push blood pressure high enough to force blood through the blocked artery. This can be diagnosed with functional tests that measure glomerular filtration rate before and after blockade of the renin-angiotensin system with angiotensin converting enzyme inhibitors or antagonists of the AT(1) subtype of the angiotensin receptor. There is insufficient data on which to make evidence-based recommendations on the management of renovascular hypertension. Only two randomised trials exist of angioplasty versus medical therapy and of these the larger was severely contaminated by angioplasty among the group initially assigned to medical therapy. Only one trial exists of angiotensin converting enzyme inhibition versus alternative medical therapy. The drugs that are most effective in medical management of renovascular hypertension--angiotensin converting enzyme inhibitors and angiotensin receptor-1 blockers--tend to be avoided because of fear of a very rare complication (acute renal failure in patients with severe stenosis of both renal arteries, or the artery to a single remaining kidney). This fear is misplaced not only because it is rare (< 5% of patients with renovascular hypertension) but because it is reversible and treatable by revascularisation. Patients with renovascular hypertension should be evaluated by nuclear medicine differential glomerular filtration rate, enhanced by blockers of the renin-angiotensin system. If medical therapy is ineffective or causes severe impairment of renal function, revascularisation is required. Some experts favour surgical revascularisation because of occasional angioplasty failure and the risk of deterioration of renal function after angioplasty.
Spence
J David
JD
Stroke Prevention & Atherosclerosis Research Centre, Roberts Research Institute, 1400 Western Rd., London, Ontario, Canada N6G 2V2. dspence@rri.ca
D058186:Acute Kidney Injury / Q000188:drug therapy / Q000503:physiopathology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D006801:Humans; D006978:Hypertension, Renovascular / Q000188:drug therapy* / Q000503:physiopathology
D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents