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Kidney Int Suppl (2011). 2011 Jun;1(1):13-16.

Major pathways of the reno-cardiovascular link: the sympathetic and renin-angiotensin systems.

Author information

1
Department of Nephrology, University Medical Center , Utrecht, The Netherlands.
2
INSERM U970, Hôpital Européen Georges Pompidou , Paris, France.
3
Department of Internal Medicine IV, Saarland University Medical Centre , Homburg/Saar, Germany.
4
ERA-EDTA Registry, Department of Medical Informatics, Academic Medical Center, University of Amsterdam , Amsterdam, The Netherlands.
5
Department of Clinical Science, Intervention and Technology, Karolinska Institutet , Stockholm, Sweden.
6
Renal Unit, Guy's and St Thomas' NHS Foundation Hospital, King's Health Partners , London, UK.
7
Division of Internal Medicine and Nephrology, Department of Nephrology, Endocrinology and Metabolic Diseases, Medical University of Silesia , Katowice, Poland.
8
Nephrology Division, Department of Medicine, Akdeniz University Medical School , Antalya, Turkey.
9
Indiana University and VAMC , Indianapolis, Indiana, USA.
10
Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Fundación Renal Iñigo Alvarez de Toledo , Madrid, Spain.
11
INSERM ERI-12 (EA 4292), Amiens and Amiens University France , Amiens, France ; Amiens University Hospital and the Jules Verne University of Picardie , Amiens, France.
12
Hospital Universitario de Bellvitge, IDIBELL, L'Hospitalet de Llobregat , Barcelona, Spain.
13
Clinic of Nephrology, C.I. Parhon University Hospital, Gr. T. Popa University of Medicine and Pharmacy , Iasi, Romania.
14
Department of Clinical Epidemiology, Leiden University Medical Center , Leiden, The Netherlands.
15
Nephrology, Dialysis and Transplantation Unit and CNR-IBIM Clinical Epidemiology and Pathophysiology of Renal Diseases and Hypertension , Reggio Calabria, Italy.

Abstract

Chronic kidney disease is often characterized by enhanced activity of the renin-angiotensin system (RAS) and the sympathetic nervous system. Independent of their effect on blood pressure, these systems also contribute to the pathogenesis of both structural and functional cardiovascular abnormalities and contribute importantly to clinical outcome. There is much evidence that the diseased kidneys are of central importance in the pathogenesis of both abnormalities. Inhibitors of the RAS also reduce sympathetic overactivity. Future research should be aimed at addressing the pathophysiological mechanisms causing the enhanced activities. Given the fact that even a small kidney lesion can cause enhanced activity of the RAS and the sympathetic nervous system, it is likely that these pathophysiological mechanisms are operational in more disease conditions, including essential hypertension, heart failure, and obesity/metabolic syndrome.

KEYWORDS:

chronic kidney disease; hypertension; renin angiotensin; sympathetic activity

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