Kinetics of carnitine concentration after switching from oral administration to intravenous injection in hemodialysis patients

Anna Suzuki,Yukinao Sakai,Kazumasa Hashimoto,Hirokazu Osawa,Shuichi Tsuruoka

doi:10.1080/0886022x.2018.1455587

Abstract

Carnitine has high dialyzability and is often deficient in dialysis patients. This deficiency is treated by either intravenous (IV) or oral supplementation of carnitine. In this study, the mode of carnitine administration was changed from oral to IV in 17 hemodialysis (HD) patients, and the treatment was discontinued after 1 year. We found that the levels of total carnitine (TC), free-carnitine (FC), and acyl-carnitine (AC) significantly increased after 3 months of switching to IV administration (p < .05). After discontinuation of carnitine administration, the TC, FC, and AC levels decreased before dialysis. The average FC value was maintained at the normal levels until 9 months, but fell below the normal values when measured at the 12th month of discontinuation. In conclusion, carnitine was maintained at significantly high levels despite the smaller dose by IV infusion as compared with that by oral administration. We therefore suggest that our results be considered while determining both the carnitine administration route and the administration period in dialysis patients under clinical settings.

Highlights

L-carnitine is a water-soluble amine present in the mitochondria of the tissues of cardiac muscle, skeletal muscle, brain, and liver, among others, as free-carnitine (FC) or acyl-carnitine (AC) [1]
Energy may be produced by beta-oxidation or through the tricarboxylic acid (TCA) cycle by conveying long-chain fatty acids through the inner mitochondrial membrane to carnitine
As carnitine is eliminated by hemodialysis (HD), dialysis patients are susceptible to carnitine deficiency and, to hypotension [3] and erythropoietin low-responsiveness anemia [4,5]

Summary

Introduction

L-carnitine is a water-soluble amine (molecular weight 162) present in the mitochondria of the tissues of cardiac muscle, skeletal muscle, brain, and liver, among others, as free-carnitine (FC) or acyl-carnitine (AC) [1]. Carnitine has high dialyzability and is often deficient in dialysis patients, because these patients are undernourished due to inflammation. Carnitine bound to acyl-coenzyme A (CoA) inhibited ATP transfer and carbohydrate metabolism, returned them to CoA and AC, and assisted in energy production by transferring them to the outside of the mitochondria [2]. Carnitine is present as FC or AC in the blood. As CoA and free CoA ratio balance is preserved, the blood AC/FC ratio shows carnitine metabolism. Carnitine deficiency causes systemic disorders such as heart failure, anemia, and muscle symptoms. As carnitine is eliminated by hemodialysis (HD), dialysis patients are susceptible to carnitine deficiency and, to hypotension [3] and erythropoietin low-responsiveness anemia [4,5]

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Results

Discussion

Conclusion