title: Atorvastatin reduces sympathetic activity in patients with chronic kidney disease.
abstract: BACKGROUND
  Hypertensive chronic kidney disease (CKD) patients often have sympathetic hyperactivity, which appears to contribute to the pathogenesis of hypertension and cardiovascular organ damage. Experimental studies and some clinical studies have shown that statin therapy can reduce central sympathetic activity. Blockade of the renin-angiotensin system (RAS), which is standard treatment for CKD, is known to lower sympathetic activity. We hypothesized that adding a statin for 6 weeks to RAS blockade would further lower sympathetic activity in hypertensive stage 2-4 CKD patients.
  
  
  METHODS
  In 10 stable CKD patients (eight men, aged 45 ± 11 years, estimated glomerular filtration rate 56 ± 22 ml/min per 1.73 m2), who were on chronic treatment with aliskiren 300 mg, blood pressure and sympathetic activity (quantified by assessment of muscle sympathetic nerve activity, MSNA) were assessed at baseline and 6 weeks after atorvastatin 20 mg/day was added. Ten other CKD patients served as time control and were studied twice with an interval of 6 weeks without any change in medication, to quantify within participant reproducibility.
  
  
  RESULTS
  Mean arterial blood pressure remained stable throughout the study (93 ± 5 versus 94 ± 5 mmHg). MSNA was reduced from 28 ± 8 to 20 ± 6 bursts/min (P = 0.01), while heart rate remained stable during the study. In the control CKD group, MSNA did not change: 26 ± 5 to 25 ± 6 bursts/min. Atorvastatin reduced total and low-density lipoprotein cholesterol.
  
  
  CONCLUSIONS
  Atorvastatin has a further sympatholytic effect in CKD patients, who are on chronic aliskiren, which is independent of blood pressure and heart rate.
authors: Department of Nephrology and Hypertension, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands.
authors: Laima
authors: L
authors: Siddiqi
authors: Jaap A
authors: JA
authors: Joles
authors: P Liam
authors: PL
authors: Oey
authors: Peter J
authors: PJ
authors: Blankestijn
mesh_terms: D000328:Adult; D000577:Amides / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects; D000069059:Atorvastatin; D001794:Blood Pressure / Q000187:drug effects; D016022:Case-Control Studies; D005260:Female; D005650:Fumarates / Q000494:pharmacology; D005919:Glomerular Filtration Rate; D006339:Heart Rate / Q000187:drug effects; D006538:Heptanoic Acids / Q000494:pharmacology*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D007676:Kidney Failure, Chronic / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects*; D013565:Sympatholytics / Q000494:pharmacology; D013997:Time Factors
chemical_list: D000577:Amides; D005650:Fumarates; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D013565:Sympatholytics; C446481:aliskiren; D000069059:Atorvastatin