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The Journal of Clinical Hypertension logoLink to The Journal of Clinical Hypertension
. 2007 May 31;3(1):53–59. doi: 10.1111/j.1524-6175.2001.00834.x

Renal Artery Stenosis in Hypertension: What about the “Other” Alternative?

Raymond R Townsend 1
PMCID: PMC8099298  PMID: 11416684

Since the introduction of reconstructive renal surgery in the 1960s and renal vessel angioplasty in the late 1970s, a large body of research literature and an interesting technology have been developed, focusing on relief for the narrowed renal artery. When renal artery stenosis (RAS) is confirmed in a hypertensive patient, often the first question asked is, “How do we plan to relieve this obstruction (or these obstructions, when multiple vessels are involved)?” Stated cynically, the presence of RAS in a hypertensive patient frequently evokes the “oculodilatory reflex” (I see it, therefore it needs dilation).

Three recent articles, 1 , 2 , 3 one of which caused a stir earlier this year, 3 have raised the issue that maybe it is time to consider the “other” alternative in hypertensive patients with RAS (where “other” is the use of current antihypertensive medicines, cessation of cigarette smoking, and lipid‐lowering therapies—also known as “medical therapy”). The reason to consider medical therapy is that angioplasty and surgery entail risks (anesthesia, bleeding, atheroembolic complications, and pseudoaneurysm formation, to name a few), and vessels subjected to angioplasty, in particular, have an irritating habit of developing restenosis in some cases, even with a properly situated stent in place.

Rather than review these three studies exhaustively, 1 , 2 , 3 let us look at the “bottom line” of what each shows. One is French, 2 one is Dutch, 3 and one is Scottish. 1 They addressed different questions in their designs, but all three were randomized studies comparing medical therapy to angioplasty in unilateral or unilateral and bilateral RAS due to atherosclerosis (they are not fibromuscular dysplasia studies).

The Webster study (Scotland) showed that the advantage of angioplasty over medical therapy in patients with bilateral RAS was limited to a modest improvement in systolic pressure control. There were no cures of hypertension in this study. The EMMA study (French) enrolled patients with unilateral RAS only and used ambulatory blood pressure monitoring and office blood pressure measurements as the outcome, measured at 6 months from randomization. The primary findings were fewer drugs needed to control blood pressure, but a higher complication rate, in the angioplasty group. Blood pressure control at 6 months was similar in the two groups, but required more medicine to achieve the same degree of control in the medical therapy group. The most controversial study was the Dutch trial, termed the DRASTIC study. In this investigation, patients who received angioplasty and those who had medical therapy had similar blood pressure control at the end of the study (at both 3 and 12 months after enrollment). However, as in the EMMA study, the angioplasty group required less medication. The controversy arose over the DRASTIC study design, which allowed subjects in the medical therapy group to cross over to the angioplasty group at 3 months if their blood pressures were still difficult to control. Keeping in mind that the design of DRASTIC specifically sought patients whose blood pressure was elevated on two drugs in the first place, it is easy to imagine that it would continue to require substantial drug therapy to maintain blood pressure if nothing other than arteriography for diagnosis of RAS is performed.

What is the lesson from all of this research? A reasonable perspective on these studies is that when we consider what to do when facing the situation of the hypertensive patient with one or more risk factors for RAS (e.g., smoking, elevation in serum creatinine, dyslipidemia, abdominal bruit, evidence of other vascular disease), we should not immediately jump to the conclusion that RAS should be sought and corrected. Of course, there are times when correction of RAS will be the best course, but the potent antihypertensive drugs we currently have, in conjunction with the ability to alter other risk factors (such as elevated lipids) should prompt us to ask ourselves whether we have fully exhausted current medical therapy before intervening further.

References

  • 1. Webster J, Marshall F, Abdalla M, et al. Randomised comparison of percutaneous angioplasty vs. continued medical therapy for hypertensive patients with atheromatous renal artery stenosis. Scottish and Newcastle Renal Artery Stenosis Collaborative Group. J Hum Hypertens. 1998;12(5):329–335. [DOI] [PubMed] [Google Scholar]
  • 2. Plouin PF, Chatellier G, Darne B, et al. Blood pressure outcome of angioplasty in atherosclerotic renal artery stenosis: A randomized trial. Essai Multicentrique Medicaments vs. Angioplastie (EMMA) Study Group. Hypertension. 1998; 31(3):823–829. [DOI] [PubMed] [Google Scholar]
  • 3. Van Jaarsveld BC, Krijnen P, Pieterman H, et al. The effect of balloon angioplasty on hypertension in atherosclerotic renal‐artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group. N Engl J Med. 2000;342(14):1007–1014. [DOI] [PubMed] [Google Scholar]

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