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Effects of Renal Denervation on Insulin Sensitivity and Inflammatory Markers in Nondiabetic Patients with Treatment-Resistant Hypertension

Increased sympathetic activity is important in the pathogenesis of hypertension and insulin resistance. Afferent signaling from the kidneys elevates the central sympathetic drive. We investigated the effect of catheter-based renal sympathetic denervation (RDN) on glucose metabolism, inflammatory mar...

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Autores principales: Kampmann, Ulla, Mathiassen, Ole N., Christensen, Kent L., Buus, Niels H., Bjerre, Mette, Vase, Henrik, Møller, Niels, Kaltoft, Anne, Poulsen, Per L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5610868/
https://www.ncbi.nlm.nih.gov/pubmed/29082259
http://dx.doi.org/10.1155/2017/6915310
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author Kampmann, Ulla
Mathiassen, Ole N.
Christensen, Kent L.
Buus, Niels H.
Bjerre, Mette
Vase, Henrik
Møller, Niels
Kaltoft, Anne
Poulsen, Per L.
author_facet Kampmann, Ulla
Mathiassen, Ole N.
Christensen, Kent L.
Buus, Niels H.
Bjerre, Mette
Vase, Henrik
Møller, Niels
Kaltoft, Anne
Poulsen, Per L.
author_sort Kampmann, Ulla
collection PubMed
description Increased sympathetic activity is important in the pathogenesis of hypertension and insulin resistance. Afferent signaling from the kidneys elevates the central sympathetic drive. We investigated the effect of catheter-based renal sympathetic denervation (RDN) on glucose metabolism, inflammatory markers, and blood pressure in nondiabetic patients with treatment-resistant hypertension. Eight subjects were included in an open-labelled study. Each patient was studied before and 6 months after RDN. Endogenous glucose production was assessed by a 3-(3)H glucose tracer, insulin sensitivity was examined by hyperinsulinemic euglycemic clamp, hormones and inflammatory markers were analyzed, and blood pressure was measured by office blood pressure readings and 24-hour ambulatory blood pressure monitoring. Insulin sensitivity (M-value) increased nonsignificantly from 2.68 ± 0.28 to 3.07 ± 0.41 (p = 0.12). A significant inverse correlation between the increase in M-value and BMI 6 months after RDN (p = 0.03) was found, suggesting beneficial effects on leaner subjects. Blood pressure decreased significantly, but there were no changes in hormones, inflammatory markers, or endogenous glucose production. Our results indicate that RDN may improve insulin sensitivity in some patients with treatment-resistant hypertension, albeit confirmation of these indications of beneficial effects on leaner subjects awaits the outcome of larger randomized controlled studies.
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spelling pubmed-56108682017-10-29 Effects of Renal Denervation on Insulin Sensitivity and Inflammatory Markers in Nondiabetic Patients with Treatment-Resistant Hypertension Kampmann, Ulla Mathiassen, Ole N. Christensen, Kent L. Buus, Niels H. Bjerre, Mette Vase, Henrik Møller, Niels Kaltoft, Anne Poulsen, Per L. J Diabetes Res Research Article Increased sympathetic activity is important in the pathogenesis of hypertension and insulin resistance. Afferent signaling from the kidneys elevates the central sympathetic drive. We investigated the effect of catheter-based renal sympathetic denervation (RDN) on glucose metabolism, inflammatory markers, and blood pressure in nondiabetic patients with treatment-resistant hypertension. Eight subjects were included in an open-labelled study. Each patient was studied before and 6 months after RDN. Endogenous glucose production was assessed by a 3-(3)H glucose tracer, insulin sensitivity was examined by hyperinsulinemic euglycemic clamp, hormones and inflammatory markers were analyzed, and blood pressure was measured by office blood pressure readings and 24-hour ambulatory blood pressure monitoring. Insulin sensitivity (M-value) increased nonsignificantly from 2.68 ± 0.28 to 3.07 ± 0.41 (p = 0.12). A significant inverse correlation between the increase in M-value and BMI 6 months after RDN (p = 0.03) was found, suggesting beneficial effects on leaner subjects. Blood pressure decreased significantly, but there were no changes in hormones, inflammatory markers, or endogenous glucose production. Our results indicate that RDN may improve insulin sensitivity in some patients with treatment-resistant hypertension, albeit confirmation of these indications of beneficial effects on leaner subjects awaits the outcome of larger randomized controlled studies. Hindawi 2017 2017-09-07 /pmc/articles/PMC5610868/ /pubmed/29082259 http://dx.doi.org/10.1155/2017/6915310 Text en Copyright © 2017 Ulla Kampmann et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Kampmann, Ulla
Mathiassen, Ole N.
Christensen, Kent L.
Buus, Niels H.
Bjerre, Mette
Vase, Henrik
Møller, Niels
Kaltoft, Anne
Poulsen, Per L.
Effects of Renal Denervation on Insulin Sensitivity and Inflammatory Markers in Nondiabetic Patients with Treatment-Resistant Hypertension
title Effects of Renal Denervation on Insulin Sensitivity and Inflammatory Markers in Nondiabetic Patients with Treatment-Resistant Hypertension
title_full Effects of Renal Denervation on Insulin Sensitivity and Inflammatory Markers in Nondiabetic Patients with Treatment-Resistant Hypertension
title_fullStr Effects of Renal Denervation on Insulin Sensitivity and Inflammatory Markers in Nondiabetic Patients with Treatment-Resistant Hypertension
title_full_unstemmed Effects of Renal Denervation on Insulin Sensitivity and Inflammatory Markers in Nondiabetic Patients with Treatment-Resistant Hypertension
title_short Effects of Renal Denervation on Insulin Sensitivity and Inflammatory Markers in Nondiabetic Patients with Treatment-Resistant Hypertension
title_sort effects of renal denervation on insulin sensitivity and inflammatory markers in nondiabetic patients with treatment-resistant hypertension
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5610868/
https://www.ncbi.nlm.nih.gov/pubmed/29082259
http://dx.doi.org/10.1155/2017/6915310
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