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Hyperlipidemia after organ transplantation.

Hyperlipidemia, long recognized as a difficult and common problem following organ transplantation, may be the underlying cause of the accelerated atherosclerosis observed in heart transplant recipients and children with renal transplants. In addition, hyperlipidemia may play a role in late renal graft loss. The cause of post-transplant hyperlipidemia is unclear. In patients treated with azathioprine and prednisone, hypertriglyceridemia is the commonest finding and probably results from an increased consumption of calories from carbohydrate and fat following resolution of uremia, in conjunction with glucose intolerance secondary to steroid administration. In patients treated with cyclosporine, hypercholesterolemia is the most common form of hyperlipidemia. Cyclosporine is a lipophilic drug that is transported in the plasma, largely in association with lipoproteins, and may require the low-density lipoprotein (LDL) receptor for internalization into cells. Hypercholesterolemia may result from interference with the basic cholesterol feedback mechanism via the LDL receptor. In addition, cyclosporine affects bile acid synthesis and worsens glucose tolerance, both factors that may promote hyperlipidemia. The first therapeutic approach to hyperlipidemia in the transplant recipient is dietary calorie-fat restriction and supplementation with soluble fiber. Ongoing clinical trials of the available pharmacologic lipid-lowering agents are addressing the safety and efficacy of these agents in the setting of immunosuppression; until that time, they should be used cautiously and in low doses.