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Sympathetic overactivity has been implicated in the pathophysiology of systemic hypertension.1,2 As shown in randomized controlled trials, percutaneous renal denervation has been proven to be an effective and safe method to treat patients with resistant hypertension.3,4 In present trials, patients with significant renal artery stenosis or abnormalities in renal artery anatomy or a history of prior renal artery intervention were excluded. Thus, no data exist regarding renal denervation in patients with accessory renal artery. Here, we report a single-sided renal denervation in an 83-year-old woman (weight, 70 kg; height, 152 cm) with contralateral accessory renal artery, who experienced medically resistant hypertension despite intake of 7 antihypertensive drugs. The patient fulfilled inclusion criteria of the Symplicity HTN-1 and HTN-2 trials.4 Secondary causes for hypertension were excluded including sleep apnea syndrome. The patient did not have diabetes, renal failure, or coronary heart disease. The patient was required to record automated home blood pressure (BP) measurements 3 times daily for periods of 7 days before and 1 and 3 months after renal denervation. Antihypertensive medication was maintained unchanged throughout follow-up. Baseline systolic/diastolic BP was 173±22 mm Hg/86±14 mm Hg. For renal denervation, the femoral artery was accessed in standard technique and fluoroscopic angiography was performed to visualize the renal artery. Angiography revealed normal configuration of left renal artery, where denervation was performed with application of 5 low-power radiofrequency treatments along the proximal portion of the vessel. Mean temperature was 48±3°C during 120 seconds of ablation at each point. On the right side, angiography revealed a cranial accessory renal artery with high ostial stenosis. The caudal renal artery showed a diameter of <4 mm precluding an ablation procedure. Because of a rather small renal artery diameter, stenting was not performed. In result, only left single-sided renal denervation was performed. After denervation, renal function assessed by serum creatinine was unchanged (baseline 74.9 μmol/L vs after 3 months 84.2 μmol/L). Single-sided renal denervation resulted in moderate office BP reduction 1 month after the procedure (173±22 mm Hg vs 162±20 mm Hg; not significant). Significant systolic BP changes were seen at 3 months follow-up of 14% (173±22 mm Hg vs 148±15 mm Hg; P<.001). Diastolic BP did not change significantly over time (86±14 mm Hg vs 83±9 mm Hg [1 month] and vs 83±9 mm Hg [3 months]). No adverse events were observed.

Our case report supports previous data on effective and significant BP reduction after renal denervation in patients with medically resistant hypertension. We describe here for the first time successful one-sided sympathetic renal denervation in a patient with an accessory renal artery showing a relevant stenosis of the ostium. Systolic BP reduction of 25 mm Hg after 3 months was comparable to the results in the randomized Symplicity HTN-1 and HTN-2 controlled trials.3,4 However, our patient had nonsignificant changes in systolic BP after 1 month and was not affected in diastolic parameters. This observation underlines the individual response of renal denervation in patients with resistant hypertension. Accessory renal arteries originating directly from the aorta were found in 25% to 50% of normal patients at autopsy.5 The accessory renal arteries were often narrower than main renal arteries. There are conflicting data whether accessory renal arteries lead to systemic arterial hypertension by activation of the renin-angiotensin system as a consequence of lower perfusion pressure and higher resistance across the accessory artery.5–8

In the present case, we found an additional, significant stenosis of the accessory renal artery. The estimated incidence of accessory renal artery stenosis ranges from 1.5% in a catheter angiography study (n=68) to 2.2% in a magnetic resonance angiography study (n=45).8,9 Controversial data suggested either transcatheter angioplasty or interventional occlusion of accessory renal arteries to treat hypertension linked to this abnormality.10 Gupta and Tello8 concluded in their study that accessory renal arteries are not associated with an increased risk of hypertension development. In our patient, we performed renal denervation only on the side with normal renal anatomy and not on the side with the accessory renal artery. Also, no dilatation or stenting of the accessory renal artery stenosis was performed due to small vessel diameter. Yet, follow-up showed a significant reduction in BP. We therefore conclude that in select patients, single-sided renal denervation may be an acceptable approach to treat resistant hypertension. Furthermore, our data support the hypothesis that accessory renal arteries may not be causative for resistant hypertension.

Disclosures:  FH has received travel expenses from Medtronic and St Jude Medical. KM has received consulting fees from Biotronik. HS has received consulting fees from AstraZeneca, Berlin-Chemie, Boehringer Ingelheim, Boston Scientific, Brahms, GlaxoSmithKline, Medtronic, MSD/Merck, Mitsubishi, Novartis, Pfizer, Sanofi-Aventis, Servier, Terumo, Actavis, Cordis, Daiichi-Sankyo, Essex, Takeda, and The Medicines Company. JW has paid consultancy with Actelion, Novartis, Pfizer, Astra-Zeneca, Medtronic, and Daiichi Sankyo.

References

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  2. References
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    Esler MD, Krum H, Sobotka PA, et al. Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomised controlled trial. Lancet. 2010;376:19031909.
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