title: Sympathetic nerve activity in end-stage renal disease.
abstract: BACKGROUND
  Uremia is proposed to increase sympathetic nerve activity (SNA) in hemodialysis patients. The aims of the present study were to determine whether reversal of uremia by successful kidney transplantation (RTX) eliminates the increased SNA and whether signals arising in the diseased kidneys contribute to the increased SNA in renal failure.
  
  
  RESULTS
  We compared muscle sympathetic nerve activity (MSNA) in 13 hemodialysis patients wait-listed for RTX and in renal transplantation patients with excellent graft function treated with cyclosporine (RTX-CSA, n=13), tacrolimus (RTX-FK, n=13), or without calcineurin inhibitors (RTX-Phi, n=6), as well as in healthy volunteers (CON, n=15). In addition to the above patients with present diseased native kidneys, we studied 16 RTX patients who had undergone bilateral nephrectomy (RTX-NE). Data are mean+/-SEM. MSNA was significantly elevated in hemodialysis patients (43+/-4 bursts/min), RTX-CSA (44+/-5 bursts/min), RTX-FK (34+/-3 bursts/min), and RTX-Phi (44+/-5 bursts/min) as compared with CON (21+/-3 bursts/min), despite excellent graft function after RTX. RTX-NE had significantly reduced MSNA (20+/-3 bursts/min) when compared with RTX patients. MSNA did not change significantly with RTX in 4 hemodialysis patients studied before and after RTX (44+/-6 versus 43+/-5 bursts/min, P=NS). In contrast, nephrectomy resulted in reduced MSNA in all 6 RTX patients studied before and after removal of the second native kidney.
  
  
  CONCLUSIONS
  Despite correction of uremia, increased SNA is observed in renal transplant recipients with diseased native kidneys at a level not significantly different from chronic hemodialysis patients. The increased SNA seems to be mediated by signals arising in the native kidneys that are independent of circulating uremia related toxins.
authors.affiliation: Department of Medicine D, University of Münster, Münster, Germany. hausber@uni-muenster.de
authors.forename: Martin
authors.initials: M
authors.lastname: Hausberg
authors.forename: Markus
authors.initials: M
authors.lastname: Kosch
authors.forename: Patrick
authors.initials: P
authors.lastname: Harmelink
authors.forename: Michael
authors.initials: M
authors.lastname: Barenbrock
authors.forename: Helge
authors.initials: H
authors.lastname: Hohage
authors.forename: Klaus
authors.initials: K
authors.lastname: Kisters
authors.forename: Karl Heinz
authors.initials: KH
authors.lastname: Dietl
authors.forename: Karl Heinz
authors.initials: KH
authors.lastname: Rahn
mesh_terms: D065095:Calcineurin Inhibitors; D016572:Cyclosporine / Q000627:therapeutic use; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007668:Kidney / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000188:drug therapy / Q000503:physiopathology* / Q000601:surgery; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000294:innervation; D009392:Nephrectomy; D006435:Renal Dialysis; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D016559:Tacrolimus / Q000627:therapeutic use; D014511:Uremia / Q000601:surgery
chemical_list: D065095:Calcineurin Inhibitors; D007166:Immunosuppressive Agents; D016572:Cyclosporine; D016559:Tacrolimus