Korean J Nephrol.
2008 May;27(3):358-363.
The Effect of Conversion from Cyclosporine to Tacrolimus in Renal Allograft Recipient with Hyperlipidemia
- Affiliations
-
- 1Department of Nephrology, College of Medicine, Kyunghee University, Seoul, Korea. kdwon@khmc.or.kr
- 2Department of Nephrology, Kyunghee East West Neo Medical Center, Seoul, Korea.
Abstract
- PURPOSE
Management of cardiovascular risk factors is of major importance in renal transplant recipients to determine long-term outcomes. While calcineurin inhibitors improve the clinical course after kidney transplantation, they have been implicated in contributing to increased cardiovascular risk. This study investigated the influence of conversion from cyclosporine to tacrolimus on cardiovascular risks and graft function in renal allograft recipients with hyperlipidemia.
METHODS
Twenty three adult renal recipients who were receiving cyclosporine-based regimen for more than one year after transplantation and had hyperlipidemia (serum total cholesterol > or =200 mg/dL) were enrolled. The effect of conversion from cyclosporine to tacrolimus was evaluated with blood pressure, fasting lipid profile, glucose and HbA1c. They were measured at baseline and at 1, 3, 6 and 12 months after conversion. The change in estimated glomerular filtration rate (eGRF) was also compared between before and after conversion.
RESULTS
Though conversion from cyclosporine to tacrolimus did not cause significant differences in the serum triglyceride level, there was a noticeable decline in total cholesterol level (213.78+/-16.28 to 185.96+/-38.62 mg/dL, p<0.01). Conversion did not trigger new onset or worsening of diabetes mellitus with no meaningful differences in fasting blood glucose and HbA1c levels. The eGFR stabilized with Tacrolimus in comparison with the cyclosporine (-2.9+/-13.4 mL/min vs. -7.3+/-13.8 mL/min).
CONCLUSION
Conversion to tacrolimus would be preferable to cyclosporine for maintenance immunesuppression in renal recipient with hyperlipidemia, as it meliorates hyperlipidemia and leads to stabilization of allograft function.