Nephrol Dial Transplant (2001) 16: 1920-1924
© 2001 European Renal Association-European Dialysis and Transplant Association
Preliminary Report
Atorvastatin improves endothelial function in renal-transplant recipients
Laboratory for Renal Physiology, Section of Nephrology, Medical Department, The National Hospital, Oslo, Norway
Background. Hyperlipidaemia and endothelial dysfunction are common features in cyclosporin A (CsA)-treated renal transplant recipients. Endothelial dysfunction may contribute to the risk of premature atherosclerosis and cardiovascular death in these patients. A beneficial effect of statin therapy beyond cholesterol lowering may be an improvement of endothelial function. The present study was designed to assess the effect of atorvastatin on serum lipids and endothelial function in CsA treated renal transplant recipients.
Methods. This pilot study was an open trial of 4 weeks atorvastatin (10 mg per day) treatment in renal transplant recipients (n=22). All patients received a CsA- and prednisolone-based immunosuppressive regimen. Endothelial function was assessed in the forearm skin microvasculature by acetylcholine stimulation and laser Doppler flowmetry, before and after atorvastatin treatment. Serum lipids, plasma endothelin-1 (ET-1), nitric oxide (NO), and von Willebrand factor (vWF) were also measured.
Results. Both total and LDL cholesterol were significantly reduced by 26.8 ± 8.4 and 41.5 ± 11.0% respectively, after 4 weeks of treatment. Endothelial function was significantly improved during atorvastatin treatment, area under the flux versus time curve (AUC)ACh was 538 ± 362 AUxmin before and 682 ± 276 AUxmin after treatment (P=0.042). Plasma NO levels also showed a borderline significant increase from 49 ± 30 to 57 ± 37 µmol/l during the treatment period (P=0.051), though plasma ET-1 (0.37±0.08 vs 0.37±0.12 fmol/ml) and vW (196±57 vs 197±37%) were unchanged.
Conclusion. Atorvastatin lowered serum cholesterol significantly and improved endothelial function in renal transplant recipients after 4 weeks of treatment. Plasma NO levels were increased during atorvastatin treatment, indicating a possible endothelial protective effect through an ‘endothelial–NO pathway’.
Keywords: atorvastatin; CsA; endothelial function; kidney; nitric oxide; transplantation
Correspondence and offprint requests to: Anders Åsberg, Laboratory for Renal Physiology, Section of Nephrology, C1 1027, Medical Department, The National Hospital, N-0027 Oslo, Norway.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  V. M. Campese and J. Park HMG-CoA Reductase Inhibitors and Renal Function Clin. J. Am. Soc. Nephrol., November 1, 2007; 2(6): 1100 - 1103. [Full Text] [PDF]
|
|
|
|
 |
|
 P. Strazzullo, S. M. Kerry, A. Barbato, M. Versiero, L. D'Elia, and F. P. Cappuccio Do Statins Reduce Blood Pressure?: A Meta-Analysis of Randomized, Controlled Trials Hypertension, April 1, 2007; 49(4): 792 - 798. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Stallone, B. Infante, A. Schena, M. Battaglia, P. Ditonno, A. Loverre, L. Gesualdo, F. P. Schena, and G. Grandaliano Rapamycin for Treatment of Chronic Allograft Nephropathy in Renal Transplant Patients J. Am. Soc. Nephrol., December 1, 2005; 16(12): 3755 - 3762. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. M. Campese, M. K. Nadim, and M. Epstein Are 3-Hydroxy-3-Methylglutaryl-CoA Reductase Inhibitors Renoprotective? J. Am. Soc. Nephrol., March 1, 2005; 16(3_suppl_1): S11 - S17. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-H. Bae, E. Bassenge, K.-Y. Kim, Y.-C. Synn, k.-R. Park, and M. Schwemmer Effects of Low-Dose Atorvastatin on Vascular Responses in Patients Undergoing Percutaneous Coronary Intervention With Stenting Journal of Cardiovascular Pharmacology and Therapeutics, July 1, 2004; 9(3): 185 - 192. [Abstract] [PDF]
|
|
|
|
|
|
W. Palinski and S. Tsimikas Immunomodulatory Effects of Statins: Mechanisms and Potential Impact on Arteriosclerosis J. Am. Soc. Nephrol., June 1, 2002; 13(6): 1673 - 1681. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Malik, D. Wichterle, V. Melenovsky, and J. Simek Von Willebrand factor and assessment of endothelial function Cardiovasc Res, April 1, 2002; 54(1): 193 - 194. [Full Text] [PDF]
|
|