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Nephrol Dial Transplant (2004) 19: 1354-1357
Nephrol Dial Transplant Vol. 19 No. 6 © ERA-EDTA 2004; all rights reserved

Editorial Comment

Sympathetic hyperactivity in chronic kidney disease

Peter J. Blankestijn

Department of Nephrology, University Medical Center Utrecht, The Netherlands

Correspondence and offprint requests to: Peter J. Blankestijn, Department of Nephrology, Room F03.226, University Medical Center, PO Box 85500, 3508 GA Utrecht, The Netherlands. Email: P.J.Blankestijn@azu.nl

Keywords: angiotensin II; chronic kidney disease; renal hypertension; sympathetic activity

The first 150 words of the full text of this article appear below.



   Introduction
 
There is clear evidence that chronic kidney disease (CKD) is often characterized by the presence of sympathetic hyperactivity. Importantly, data are accumulating that this sympathetic hyperactivity is indeed important, because it may influence cardiovascular and renal prognosis. Comprehensive reviews have been published elsewhere [1,2]. The purpose of this Editorial Comment is to briefly summarize available knowledge on the pathogenesis of sympathetic hyperactivity and to discuss its clinical relevance, the consequences of this knowledge for the choice of treatment and as yet unresolved issues.



   Pathogenesis
 
Already in the 1970s, increased catecholamine levels, as an index for sympathetic activity, were reported in CKD patients. With the microneurographic technique, true sympathetic nerve activity can be measured, usually as muscle sympathetic nerve activity (MSNA). This MSNA, for instance measured in the peroneal nerve, represents the centrally generated sympathetic nerve activity directed to resistance vasculature. Sympathetic activity is not uniform in all . . . [Full Text of this Article]



   Clinical relevance
 
Hypertension
Cardiovascular outcome
Kidney damage


   Treatment
 


   Unresolved issues
 


   Conclusion
 

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