O108
ENDOVASCULAR RENAL DENERVATION IN DIALYSIS-DEPENDENT RENAL
FAILURE TO REDUCE CARDIOVASCULAR RISK
Hoye N. A.1, Baldi, J. C.1, Jardine D. L.2, Wilkins, G. T.1, Wilson, L. C.1, Walker, R. J.1
1
Department of Medicine, Dunedin School of Medicine, University of Otago, Dunedin,
New Zealand
2
Department of Medicine, Christchurch School of Medicine and Health Sciences,
University of Otago, Christchurch, New Zealand
INTRODUCTION: Endovascular renal denervation is a catheter-based treatment for
resistant hypertension that reduces afferent and efferent renal sympathetic nerve activity1,2. In
chronic kidney disease, elevated sympathetic activity has been causally linked to disease
progression3 and cardiovascular sequelae4,5. We hypothesized that renal denervation in
dialysis patients would reduce muscle sympathetic nerve activity (MSNA) resulting in
reduced blood pressure (BP) and cardiovascular risk.
METHODS: One hundred and three dialysis patients were screened for uncontrolled BP
(office BP > 140/90 mmHg despite clinical normovolaemia, whilst taking two or more antihypertensives at maximal tolerated doses). Nine patients were recruited into the trial. Office
and ambulatory blood pressure monitoring (ABPM) were performed at baseline and one and
three months post denervation, along with recordings of supine MSNA6. Bioimpedance
spectroscopy was also recorded at similar time points to formalize patients’ volume status.
Bilateral renal denervation was performed as described previously7.
RESULTS: Office BP reduced from 179±28/90±17mmHg at baseline to 156±24/74±14
mmHg at one month and 153±25/83±12mmHg at three months. The effect on ABPM was
attenuated, with a reduction from 173±19/92±11mmHg at baseline to 173±23/89±13 mmHg
at one month and 165±25/87±11 at three months. All in all, only office systolic blood
pressure had a statistically significant reduction by repeated measures analysis of variance
(p=0.036). This is in keeping with the only other published case series of renal denervation in
dialysis patients8. Although a reduction in BP was noted, MSNA did not change (58.8±12.4
bursts/min at baseline, 58.8±14.9 bursts/min at one month and 58.9±13.2 at three months,
p=0.872). There was also no observed change in hydration status (3.2±1.7L over-hydrated at
baseline, 4.0±2.2L at one month, 3.0±2.4L at three months, p=0.148). One patient developed
a pseudoaneurysm at the site of femoral artery puncture that needed surgical repair, another
suffered a myocardial infarction four days post procedure, one more developed unstable
angina at three months.
CONCLUSIONS: Renal denervation may not represent the panacea many are billing it as.
We could not find supportive evidence that it reduces the significant sympathetic overload
seen in chronic kidney disease. The underlying mechanism for its seemingly volumeindependent blood pressure lowering effects needs further research. An elevated risk of periprocedural complications may also exist in this population.
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Engl J Med. 2009;361(9):932–4.
2. Hering D, Lambert EA, Marusic P, et al. Substantial reduction in single sympathetic nerve firing after renal denervation in
patients with resistant hypertension. Hypertension. 2013;61(2):457–64.
3. Grassi G, Quarti-Trevano F, Seravalle G, et al. Early sympathetic activation in the initial clinical stages of chronic renal
failure. Hypertension. 2011;57(4):846–51.
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Disease. Circulation. 2002;105(11):1354–1359.
5. Herzog CA, Mangrum JM, Passman R. Sudden cardiac death and dialysis patients. Semin. Dial. 2008;21(4):300–7.
6. Sundlöf G, Wallin B. Human muscle nerve sympathetic activity at rest. Relationship to blood pressure and age. J. Physiol.
1978;274:621–637.
7. Worthley SG, Tsioufis CP, Worthley MI, et al. Safety and efficacy of a multi-electrode renal sympathetic denervation system
in resistant hypertension: the EnligHTN I trial. Eur Hear. J. 2013;34(28):2132-2140.
8. Schlaich MP, Bart B, Hering D, et al. Feasibility of catheter-based renal nerve ablation and effects on sympathetic nerve
activity and blood pressure in patients with end-stage renal disease. Int J Cardiol. 2013;168(3):2214–2220.