Abstract
Hyperlipidemia is an important complication of solid-organ transplantation, affecting up to 80% of heart [1] and 75% of kidney [2] transplant recipients. The potential causes of hyperlipidemia in transplant recipients include dietary indiscretion secondary to prednisone therapy and an improved sense of well-being in the posttransplant period, genetic predisposition and side-effects of both prednisone and cyclosporin. The possible consequences of posttransplant hyperlipidemia include an increased risk for both cardiovascular morbidity and mortality and the development of chronic rejection. Kidney transplant recipients are at high risk for the development of ischemic heart disease, peripheral vascular disease and cerebrovascular disease [3]. It has been reported that 55% of deaths in renal transplant recipients with functioning grafts were cardiovascular in nature [4], In addition to the cardiovascular risk of posttransplant hyperlipidemia, there is growing evidence suggesting a correlation between high lipid levels and the development of chronic rejection (or allograft vasculopathy) after kidney [5–7] and heart [8] transplantation.
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Katznelson, S., Kobashigawa, J.A. (1997). The effects of HMG-CoA reductase inhibitors after kidney and heart transplantation: Lipid lowering and immunosuppression. In: Touraine, J.L., Traeger, J., Bétuel, H., Dubernard, J.M., Revillard, J.P., Dupuy, C. (eds) Late Graft Loss. Transplantation and Clinical Immunology, vol 28. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5434-5_19
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DOI: https://doi.org/10.1007/978-94-011-5434-5_19
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