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Lovastatin treatment of hypercholesterolemia in renal transplant recipients
B L Kasiske1, K L Tortorice, K L Heim-Duthoy
1Department of Medicine, Hennepin County Medical Center, Minneapolis, Minnesota 55415.
Insights
Lovastatin effectively treats hypercholesterolemia in renal transplant patients, significantly reducing total and LDL cholesterol. This HMG-CoA reductase inhibitor shows promise for improving lipid profiles in transplant recipients on immunosuppression.
Area of Science:
- Nephrology
- Cardiology
- Pharmacology
Background:
- Hypercholesterolemia management is challenging in renal transplant recipients.
- Patients often require long-term immunosuppression, which can affect lipid metabolism.
Purpose of the Study:
- To evaluate the efficacy and safety of lovastatin in treating hypercholesterolemia in renal transplant recipients.
- To assess the impact of lovastatin on lipid profiles and immunosuppressive therapy.
Main Methods:
- Double-blind, randomized crossover study involving 11 renal transplant recipients.
- Patients received diet therapy followed by lovastatin (20 mg/day) or placebo for 6 weeks, with a crossover period.
- Stable allograft function and conventional immunosuppression (prednisone, azathioprine) were maintained.
Main Results:
- Lovastatin significantly reduced total cholesterol by 21% (P < 0.05) and LDL cholesterol by 28% (P < 0.05).
- No statistically significant changes were observed in HDL cholesterol, triglycerides, or apolipoproteins.
- Liver enzymes, creatine phosphokinase, and renal function remained stable.
- A significant increase in white blood cell count (27%) and neutrophils (45%) was noted with lovastatin (P < 0.05).
Conclusions:
- Lovastatin is a safe and effective treatment for hypercholesterolemia in renal transplant recipients on conventional immunosuppression.
- The observed increase in WBC may suggest a beneficial interaction with azathioprine, potentially mitigating bone marrow suppression.
Abstract:
The treatment of hypercholesterolemia in renal transplant recipients has been problematic. In the present double-blind study, 11 patients were treated with diet for at least 4 weeks. They were then randomized to placebo or the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, lovastatin (20 mg/day) for 6 weeks, followed by crossover to an additional 6 weeks of lovastatin or placebo. All patients had stable allograft function 8.4 +/- 1.2 years (mean +/- SEM) after transplantation, and received low-dose prednisone and azathioprine immunosuppression. Compared with diet alone, lovastatin caused a 21% reduction in total cholesterol from 307 +/- 14 mg/dL to 244 +/- 13 mg/dL (P less than 0.05). Lovastatin reduced LDL cholesterol 28% from 214 +/- 12 mg/dL to 155 +/- 11 mg/dL (P less than 0.05). Trends toward favorable changes in HDL cholesterol, serum triglycerides, and apolipoproteins were not statistically significant. Liver enzymes, creatine phosphokinase, and renal function remained stable. With lovastatin there was a 27% increase in the WBC (from 6220 +/- 530 cells/mm3 to 7780 +/- 510 cells/mm3, P less than 0.05) that was attributable to a 45% increase in neutrophils (P less than 0.05). This effect of lovastatin, possibly the result of reduced azathioprine bone marrow suppression, could have important implications for immunosuppressive therapy in this patient population. Altogether, these results suggest that lovastatin may be a safe and effective treatment for hypercholesterolemia in renal transplant recipients receiving conventional immunosuppression.