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Endovascular Renal Denervation in End-Stage Kidney Disease Patients: Cardiovascular Protection—A Proof-of-Concept Study
INTRODUCTION: Sympathetic neural activation is markedly increased in end-stage kidney disease (ESKD). Catheter-based renal denervation (RDN) reduces sympathetic overactivity and blood pressure in resistant hypertension. We investigated the effect of RDN on sympathetic neural activation and left vent...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Elsevier
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5733679/ https://www.ncbi.nlm.nih.gov/pubmed/29270493 http://dx.doi.org/10.1016/j.ekir.2017.04.012 |
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author | Hoye, Neil A. Wilson, Luke C. Wilkins, Gerard T. Jardine, David L. Putt, Tracey L. Samaranayaka, Ari Schollum, John B.W. Walker, Robert J. |
author_facet | Hoye, Neil A. Wilson, Luke C. Wilkins, Gerard T. Jardine, David L. Putt, Tracey L. Samaranayaka, Ari Schollum, John B.W. Walker, Robert J. |
author_sort | Hoye, Neil A. |
collection | PubMed |
description | INTRODUCTION: Sympathetic neural activation is markedly increased in end-stage kidney disease (ESKD). Catheter-based renal denervation (RDN) reduces sympathetic overactivity and blood pressure in resistant hypertension. We investigated the effect of RDN on sympathetic neural activation and left ventricular mass in patients with ESKD. METHODS: Nine ESKD (6 hemodialysis and 3 peritoneal dialysis) patients with dialysis vintage of ≥11 months were treated with RDN (EnligHTN system). Data were obtained on a nondialysis day; at baseline, 1, 3, and 12 months post-RDN. RESULTS: At baseline sympathetic neural activation measured by muscle sympathetic nervous activity (MSNA) and plasma norepinephrine concentrations were markedly elevated. Left ventricular hypertrophy (LVH) was evident in 8 of the 9 patients. At 12 months post-RDN, blind analysis revealed that MSNA(frequency) (–12.2 bursts/min(1), 95% CI [–13.6, –10.7]) and LV mass (–27 g/m(2), 95% CI [–47, –8]) were reduced. Mean ambulatory BP (systolic: –24 mm Hg, 95% CI [–42, –5] and diastolic: –13 mm Hg, 95% CI [–22, –4]) was also reduced at 12 months. Office BP was reduced as early as 1 month (systolic: –25 mm Hg, 95% CI [–45, –5] and diastolic: –13 mm Hg, 95% CI [–24, –1]). Both ambulatory and office BP had clinically significant reductions in at least 50% of patients out to 12 months. DISCUSSION: Catheter-based RDN significantly reduced MSNA and LV mass as well as systemic BP in this group of patients with ESKD. |
format | Online Article Text |
id | pubmed-5733679 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-57336792017-12-21 Endovascular Renal Denervation in End-Stage Kidney Disease Patients: Cardiovascular Protection—A Proof-of-Concept Study Hoye, Neil A. Wilson, Luke C. Wilkins, Gerard T. Jardine, David L. Putt, Tracey L. Samaranayaka, Ari Schollum, John B.W. Walker, Robert J. Kidney Int Rep Clinical Research INTRODUCTION: Sympathetic neural activation is markedly increased in end-stage kidney disease (ESKD). Catheter-based renal denervation (RDN) reduces sympathetic overactivity and blood pressure in resistant hypertension. We investigated the effect of RDN on sympathetic neural activation and left ventricular mass in patients with ESKD. METHODS: Nine ESKD (6 hemodialysis and 3 peritoneal dialysis) patients with dialysis vintage of ≥11 months were treated with RDN (EnligHTN system). Data were obtained on a nondialysis day; at baseline, 1, 3, and 12 months post-RDN. RESULTS: At baseline sympathetic neural activation measured by muscle sympathetic nervous activity (MSNA) and plasma norepinephrine concentrations were markedly elevated. Left ventricular hypertrophy (LVH) was evident in 8 of the 9 patients. At 12 months post-RDN, blind analysis revealed that MSNA(frequency) (–12.2 bursts/min(1), 95% CI [–13.6, –10.7]) and LV mass (–27 g/m(2), 95% CI [–47, –8]) were reduced. Mean ambulatory BP (systolic: –24 mm Hg, 95% CI [–42, –5] and diastolic: –13 mm Hg, 95% CI [–22, –4]) was also reduced at 12 months. Office BP was reduced as early as 1 month (systolic: –25 mm Hg, 95% CI [–45, –5] and diastolic: –13 mm Hg, 95% CI [–24, –1]). Both ambulatory and office BP had clinically significant reductions in at least 50% of patients out to 12 months. DISCUSSION: Catheter-based RDN significantly reduced MSNA and LV mass as well as systemic BP in this group of patients with ESKD. Elsevier 2017-05-04 /pmc/articles/PMC5733679/ /pubmed/29270493 http://dx.doi.org/10.1016/j.ekir.2017.04.012 Text en © 2017 International Society of Nephrology. Published by Elsevier Inc. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Clinical Research Hoye, Neil A. Wilson, Luke C. Wilkins, Gerard T. Jardine, David L. Putt, Tracey L. Samaranayaka, Ari Schollum, John B.W. Walker, Robert J. Endovascular Renal Denervation in End-Stage Kidney Disease Patients: Cardiovascular Protection—A Proof-of-Concept Study |
title | Endovascular Renal Denervation in End-Stage Kidney Disease Patients: Cardiovascular Protection—A Proof-of-Concept Study |
title_full | Endovascular Renal Denervation in End-Stage Kidney Disease Patients: Cardiovascular Protection—A Proof-of-Concept Study |
title_fullStr | Endovascular Renal Denervation in End-Stage Kidney Disease Patients: Cardiovascular Protection—A Proof-of-Concept Study |
title_full_unstemmed | Endovascular Renal Denervation in End-Stage Kidney Disease Patients: Cardiovascular Protection—A Proof-of-Concept Study |
title_short | Endovascular Renal Denervation in End-Stage Kidney Disease Patients: Cardiovascular Protection—A Proof-of-Concept Study |
title_sort | endovascular renal denervation in end-stage kidney disease patients: cardiovascular protection—a proof-of-concept study |
topic | Clinical Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5733679/ https://www.ncbi.nlm.nih.gov/pubmed/29270493 http://dx.doi.org/10.1016/j.ekir.2017.04.012 |
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