Sympathetic activation in chronic renal failure

J Am Soc Nephrol. 2009 May;20(5):933-9. doi: 10.1681/ASN.2008040402. Epub 2008 Sep 17.

Abstract

The potential involvement of sympathetic overactivity has been neglected in this population despite accumulating experimental and clinical evidence suggesting a crucial role of sympathetic activation for both progression of renal failure and the high rate of cardiovascular events in patients with chronic kidney disease. The contribution of sympathetic neural mechanisms to the occurrence of cardiac arrhythmias, the development of hypertension, and the progression of heart failure are well established; however, the exact mechanisms contributing to heightened sympathetic tone in patients with chronic kidney disease are unclear. This review analyses potential mechanisms underlying sympathetic activation in chronic kidney disease, the range of adverse consequences associated with this activation, and potential therapeutic implications resulting from this relationship.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases / epidemiology
  • Cardiovascular Diseases / mortality
  • Catecholamines / blood
  • Clonidine / therapeutic use
  • Debrisoquin / therapeutic use
  • Disease Models, Animal
  • Efferent Pathways / physiopathology
  • Humans
  • Hypertension / drug therapy
  • Hypertension / epidemiology
  • Hypertension / mortality
  • Kidney / innervation
  • Kidney Failure, Chronic / complications*
  • Kidney Failure, Chronic / epidemiology
  • Kidney Failure, Chronic / physiopathology*
  • Monoamine Oxidase / deficiency
  • Monoamine Oxidase / metabolism
  • Nerve Fibers / physiology
  • Nitric Oxide / physiology
  • Norepinephrine / therapeutic use
  • Sympathetic Nervous System / physiopathology*

Substances

  • Catecholamines
  • Nitric Oxide
  • Monoamine Oxidase
  • renalase
  • Clonidine
  • Debrisoquin
  • Norepinephrine