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Review
. 2023 Aug 29;12(17):5634.
doi: 10.3390/jcm12175634.

Renal Denervation as a Complementary Treatment Option for Uncontrolled Arterial Hypertension: A Situation Assessment

Affiliations
Review

Renal Denervation as a Complementary Treatment Option for Uncontrolled Arterial Hypertension: A Situation Assessment

Max Wagener et al. J Clin Med. .

Abstract

Uncontrolled arterial hypertension is a major global health issue. Catheter-based renal denervation has shown to lower blood pressure in sham-controlled trials and represents a device-based, complementary treatment option for hypertension. In this situation assessment, the authors, who are practicing experts in hypertension, nephrology, general practice and cardiology in the Republic of Ireland, discuss the current evidence base for the BP-lowering efficacy and safety of catheter-based renal denervation with different modalities. Although important questions remain regarding the identification of responders, and long-term efficacy and safety of the intervention, renal denervation has the potential to provide much-needed help to address hypertension and its adverse consequences. The therapeutic approach needs to be multidisciplinary and personalised to take into account the perspective of patients and healthcare professionals in a shared decision-making process.

Keywords: arterial hypertension; renal denervation; resistant hypertension; uncontrolled hypertension.

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Conflict of interest statement

Max Wagener has received educational support from Medtronic. Faisal Sharif has received consultancy fees from Medtronic. Faisal Sharif has received research funding from Boston Scientific, Endotronix and Medtronic. James Shand has received consultancy fees from Medtronic and Shockwave Medical. E. Dolan, S. Arnous, J. Galvin, A. W Murphy, I Casserly, J. Eustace, S. O’Connor, C. McCreery, C. Wall and S. Mathiullah have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Effects of renal nerve stimulation on plasma renin activity (PRA), glomerular filtration rate (GFR), renal blood flow (RBF) and fractional excretion of sodium (FENA). From Johns et al. (Compr Physiol 2011;1:731–767) [21].
Figure 2
Figure 2
(a) Change in SBP as assessed by ABPM. Data represented by trial-defined primary efficacy endpoints. (°) Change in 24 h systolic BP as assessed by ABPM. (*) Change in daytime systolic BP as assessed by ABPM. (b) Change in systolic office BP from baseline to trial-defined primary endpoint time at 2 (*), 3 (°) and 6 (“) months.
Figure 2
Figure 2
(a) Change in SBP as assessed by ABPM. Data represented by trial-defined primary efficacy endpoints. (°) Change in 24 h systolic BP as assessed by ABPM. (*) Change in daytime systolic BP as assessed by ABPM. (b) Change in systolic office BP from baseline to trial-defined primary endpoint time at 2 (*), 3 (°) and 6 (“) months.
Figure 3
Figure 3
Relative Risk Reduction in adverse outcomes with sustained reductions in systolic BP by 5 (orange) and 10 (green) mmHg. Adapted from Lancet. 2016;387(10022):957–967 [3] and Lancet. 2021;397(10285):1625–1636 [67] (* reduction in all-cause mortality not significant (RR 0.98, 95%CI 0.96–1.01) for –5 mmHg reduction in SBP, but CV mortality significantly reduced RR 0.95 (95% CI 0.92–0.99).

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