title: Sympathetic hyperactivity and clinical outcome in chronic kidney disease patients during standard treatment.
abstract: BACKGROUND
  Sympathetic hyperactivity has been associated with adverse clinical outcome and is common in patients with chronic kidney disease (CKD). Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARB) have been shown to reduce sympathetic activity in CKD patients. The present study was performed to investigate whether sympathetic hyperactivity was related to clinical outcome in CKD patients treated with ACEi or ARB.
  
  
  METHODS
  Muscle sympathetic nerve activity (MSNA) was measured in 66 nondiabetic patients (70% men) with CKD, median age 47 years (range 21-65) and mean estimated glomerular filtration rate (eGFR) 39+/-29 ml/min per 1.73 m2. Patients were followed up for a median 78 months (range 6-123), and subsequent clinical events were recorded.
  
  
  RESULTS
  During follow-up, average blood pressure was 131+/-11 mm Hg systolic and 83+/-6 mm Hg diastolic. Twenty-one events (4 deaths and 17 nonfatal cardiovascular events) occurred in 16 patients. MSNA among the group with events was 40+/-18 bursts/min, compared with 30+/-11 bursts/min in those with no events (p=0.009). An increase of MSNA of 10 bursts/min was related to an increased risk of an event (hazard ratio=1.6; 95% confidence interval, 1.0-2.8; p=0.08), independent of GFR and blood pressure. Age attenuated this relation.
  
  
  CONCLUSIONS
  Sympathetic hyperactivity was associated with the composite of all-cause mortality and nonfatal cardiovascular events in CKD patients, despite treatment with ACEi or ARB. Further studies to investigate potential effects of additional sympatholytic therapy in these patients are warrented.
authors.affiliation: Department of Nephrology, University Medical Center Utrecht, Utrecht, The Netherlands.
authors.forename: E Lars
authors.initials: EL
authors.lastname: Penne
authors.forename: Jutta
authors.initials: J
authors.lastname: Neumann
authors.forename: Inge H
authors.initials: IH
authors.lastname: Klein
authors.forename: P Liam
authors.initials: PL
authors.lastname: Oey
authors.forename: Michiel L
authors.initials: ML
authors.lastname: Bots
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Blankestijn
mesh_terms: D000328:Adult; D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001342:Autonomic Nervous System Diseases / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013565:Sympatholytics / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D013565:Sympatholytics