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Nephrol Dial Transplant (2000) 15: 755-758
© 2000 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Sympathetic overactivity in renal failure controlled by ACE inhibition: clinical significance

Peter J. Blankestijn, Gerry Ligtenberg, Inge H. H. T. Klein and Hein A. Koomans

Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands

Introduction

We have recently shown that sympathetic activity is increased in patients with chronic renal failure (CRF), and that this can be controlled by enalapril, but not by amlodipine [1]. What can we learn from these data and do they affect our daily clinical practice?

Sympathetic overactivity in CRF

Is it news that sympathetic activity is high in patients with CRF? Certainly not. The subject was recently reviewed in this journal and elsewhere [2,3], although the information that we had until recently was quite indirect. It was known for a long time that plasma catecholamine concentrations are approximately doubled in CRF patients [4,5], but this could also be due to the reduced clearance of catecholamines by the kidney. Although the method of measuring muscle sympathetic nerve activity (MSNA) directly in humans was available in the late seventies, the first publication showing that MSNA was increased . . . [Full Text of this Article]

Pathophysiology of sympathetic overactivity in CRF

How can ACE inhibition lower sympathetic activity?

Clinical importance of control of sympathetic overactivity

Future directions

Conclusion

Acknowledgments

Notes

References


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