Hypertriglyceridemia is often present in chronically uremic patients treated with maintenance hemodialysis and has been considered a risk factor in the accelerated development of atheroma. Muscle carnitine content is low in hemodialyzed patients. This abnormality may help to explain the myopathy and cardiomyopathy often observed in these subjects. In addition, carnitine might play a role in the hypertriglyceridemia in renal failure. Carnitine, which is necessary for fatty acid oxidation, has been recently reported to lower serum triglycerides in patients with type IV hyperlipoproteinemia. Carnitine was administered intravenously three times weekly at the end of hemodialysis in eight patients. Carnitine was given in 0.5 g doses for 8 weeks and then in 1.0 g doses for 6 additional weeks. There was a significant decrease in serum triglycerides at the end of treatment. In contrast, serum lipids in eight hemodialysis patients receiving placebo did not change significantly. Carnitine administration does not cause any side effect except some euphoria. These results suggest that carnitine may be effective in the treatment of hypertriglyceridemia in dialysis patients.

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1. Acetylcarnitine added in catalytic amounts to kidney mitochondria produces an active oxidation of endogenous fatty acids. 2. In conditions of mitochondrial ;aging', under which acetate is not oxidized, acetylcarnitine also promotes the oxidation of this exogenous substrate. 3. Dinitrophenol completely abolishes the action of acetylcarnitine. 4. Carnitine is ineffective both in the oxidation of endogenous fatty acids and of exogenous acetate. 5. The action of acetylcarnitine is shared, though to a smaller extent, by pyruvate. 6. The mechanism of acetylcarnitine action has been interpreted by considering that the readily oxidizable acetyl group of acetylcarnitine can supply the initial investment of energy needed to start fatty acid oxidation.

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