CASE REPORTS Renal Arterial Intervention and Angiotensin Blockade in Atherosclerotic Nephropathy David J.A. Goldsmith, FRCP, John Reidy, FRCR, and John Scoble, FRCP ● Atherosclerotic renal arterial disease (ARAD) is becoming a more important cause of end-stage renal failure. Diagnosis is more easily achieved because of greater clinical suspicion and more refined screening tools. However, the medical and interventional management of patients with ARAD is not well defined in the literature because there have been few randomized trials. Because the use of angiotensin-converting enzymes (ACE) inhibitors, and more recently angiotensin-antagonists, has become much more widespread, it is inevitable that we should, knowingly or not, give these drugs to patients with ARAD. We describe 2 case studies in which the angiotensin-antagonist irbesartan was given to 2 patients with effectively single-functional kidneys after successful renal arterial radiologic intervention. The rationale for the use of irbesartan was to control BP, which had not responded to the initial arterial intervention, and took place in patients both refractory to, and intolerant of, many other anti-hypertensive drugs. Irbesartan successfully and safely reduced systemic BP, measured by use of ambulatory BP, without prejudicing renal function (measured by use of individual kidney function GFR). © 2000 by the National Kidney Foundation, Inc. INDEX WORDS: Renal artery; angioplasty; stent; angiotensin antagonism; blood pressure. A THEROSCLEROTIC renal arterial stenosis (ARAS) is a rare but important cause of secondary hypertension, and a significant cause of end-stage renal failure. 1 One of the several modes of presentation of ARAS is raised blood pressure (BP), which often is resistant to antihy- pertensive drug treatment. The effect of renal arterial interventions (angioplasty, arterial stent- ing, surgery) on established raised BP in ARAS is generally disappointing, although such inter- ventions do have a role in preserving functional renal mass. 2-4 Hypertension is a major risk factor for coronary and cerebral events, and recent trials have indicated that progressively more suc- cessful treatment is achieved pari passu with BP reduction at least down to levels of 130 to 140/80 to 90 mm Hg. 5-8 To achieve these BP levels in ARAS patients is very challenging and should be the subject of a randomized controlled trial, but given the very high mortality of such patients on dialysis programs, 1,9 the deleterious effect of raised BP on residual renal function in chronic renal failure, 10 and the protective effect on renal function of angiotensin-converting enzyme (ACE) inhibitors in proteinuric diabetic and non- diabetic chronic renal failure, 11-13 it is both intui- tive and logical to intervene to try to reduce BP significantly in these patients for both renal and nonrenal reasons. The use of ACE inhibitors and angiotensin antagonists, potent antihypertensive drugs with a marked ability to reverse left ventricular hyper- trophy (LVH), 14,15 is complicated, in the context of renovascular disease, by their propensity to reduce glomerular filtration in hemodynamically severe renal arterial stenosis, in which efferent renal arteriolar tone, on which renal filtration depends, is exquisitely sensitive to circulating angiotensin. This is a well-known cause of acute renal failure. 16 We describe the sequential intervention of renal arterial angioplasty/stenting to preserve re- nal blood supply and functional renal mass. The procedure also was undertaken to reduce the degree of arterial stenosis away from the severity range at which acute renal functional disturbance with angiotensin antagonism is likely. Cautious use of a potent selective angiotensin II receptor antagonist also was used to engineer a significant decrease in systemic BP without prejudicing re- nal function in two patients refractory to, or intolerant of, other antihypertensive drugs. From the Departments of Renal Medicine and Radiology, Guy’s Hospital, London, United Kingdom. Received January 24, 2000; accepted in revised form April 21, 2000. Address reprint requests to David J.A. Goldsmith, FRCP, Renal Unit, 4 th Floor Thomas Guy House, Guy’s Hospi- tal, London SE1 9RT, United Kingdom. E-mail: David. goldsmith@gstt. sthames.nhs.uk © 2000 by the National Kidney Foundation, Inc. 0272-6386/00/3604-0022$3.00/0 doi:10.1053/ajkd.2000.17686 American Journal of Kidney Diseases, Vol 36, No 4 (October), 2000: pp 837-843 837