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      Effect of L-carnitine on the serum lipoproteins and HDL-C subclasses in hemodialysis patients.

      Nephron. Clinical practice
      Adult, Animals, Carnitine, therapeutic use, Cholesterol, HDL, blood, Cholesterol, VLDL, Female, Humans, Kidney Failure, Chronic, therapy, Lipoproteins, Male, Middle Aged, Renal Dialysis, Triglycerides

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          Abstract

          Following carnitine administration a decrease in plasma levels of triglyceride (TG) and increase in total high-density lipoprotein cholesterol (HDL-C) has been reported. Our hypothesis was that it also improves the HDL2/HDL3 ratio, symptomatic intradialytic hypotension, and anemia in hemodialysis (HD) patients. Forty HD patients with a mean (+/- SD) age of 53 +/- 13 years were treated with 500 mg/day carnitine taken orally for 2 months. Patients were used as their own controls (before treatment). Lipid and lipoproteins were determined by Alcyon Abbott autoanalyzer. HDL subclasses were measured by magnesium precipitation after fractionation with dextran sulfate. Hemoglobin, hematocrit and serum albumin were measured by standard methods. The results were analyzed by SPSS 11.05. We found a significant decrease in serum TG (2.22 +/- 0.99 vs. 1.93 +/- 1.07 mmol/l, p < 0.01) and VLDL-C (0.93 +/- 0.36 vs. 0.81 +/- 0.34 mmol/l, p = 0.01) and a marked increase in HDL-C (0.9 +/- 0.16 vs. 1.06 +/- 0.24 mmol/l, p < 0.05), HDL2-C (0.17 +/- 0.06 vs. 0.27 +/- 0.14 mmol/l, p < 0.05) and albumin (37 +/- 4 vs. 42 +/- 5 g/l, p = 0.01) levels. The serum levels of total cholesterol (4.61 +/- 0.89 vs. 4.5 +/- 0.95 mmol/l, p = 0.1), LDL-C (2.78 +/- 0.85 vs. 2.6 +/- 0.89 mmol/l, p > 0.05), HDL3-C (0.73 +/- 0.1 vs. 0.79 +/- 0.17 mmol/l, p > 0.05), hemoglobin, hematocrit, and intradialytic blood pressure did not change after the treatment. Treatment with 500 mg/day carnitine taken orally for 2 months reduces serum levels of TG and VLDL-C, and increases HDL-C, HDL2-C and albumin in HD patients. Copyright 2005 S. Karger AG, Basel.

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          Lipids and risk of coronary heart disease The Framingham Study

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            Dialysis-related carnitine disorder and levocarnitine pharmacology.

            Among the homeostatic processes controlling the endogenous L-carnitine pool in humans, the kidney has a vital role through extensive and adaptive tubular reabsorption. Kidney disease can lead to disturbances in L-carnitine homeostasis, and long-term hemodialysis therapy can lead to a significant reduction in plasma and tissue L-carnitine levels and an increase in the ratio of acyl-L-carnitine to free L-carnitine. These alterations may interfere with the oxidation of fatty acids and removal from tissues of unwanted short-chain acyl groups. A dialysis-related carnitine disorder (DCD) arises when these biochemical abnormalities exist in association with such clinical symptoms as muscle weakness, cardiomyopathy, intradialytic hypotension, or anemia that is resistant to erythropoietin therapy. Exogenous L-carnitine, administered intravenously, is approved for the treatment of secondary carnitine deficiency caused by long-term hemodialysis. Although intravenous administration of 20-mg/kg doses at the end of each hemodialysis session leads to supraphysiological levels of the compound in plasma, these levels do not appear to be associated with adverse effects. Because more than 99% of the body's carnitine pool is located outside of plasma, supraphysiological plasma levels appear to be required to ensure that depleted muscle stores can be replenished. Although oral L-carnitine has been used for the treatment of DCD, the bioavailability of oral L-carnitine is low (<15%) in healthy subjects and unknown in patients with end-stage renal disease. Moreover, gastrointestinal degradation of L-carnitine to trimethylamine and other compounds might limit the usefulness of long-term oral L-carnitine administration in this patient group.
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              Multicenter trial of L-carnitine in maintenance hemodialysis patients. II. Clinical and biochemical effects.

              Since carnitine deficiency has been reported in some patients undergoing maintenance hemodialysis, we studied the effects of intravenous infusion of L-carnitine or placebo at the end of each dialysis treatment. The trial, which lasted seven months (one month baseline, 6 months treatment) was multicenter, double blind, placebo controlled, and randomized. Eighty-two long-term hemodialysis patients, who were given either carnitine (N = 38) or placebo (N = 44), completed this study. In each group, clinical and biochemical parameters during treatment were compared with baseline values. Intra-dialytic hypotension and muscle cramps were reduced only in the carnitine treated group, while improvement in post-dialysis asthenia was noticed in both carnitine and placebo groups. Maximal oxygen consumption, measured during a progressive work exercise test, improved significantly in the carnitine group (111 +/- 50 ml/min. P less than 0.03) and was unchanged in the placebo group. L-carnitine treatment was associated with a significant drop in pre-dialysis concentrations of serum urea nitrogen, creatinine and phosphorus (means +/- SEM, 101 +/- 4.5 to 84 +/- 3.9, 16.7 +/- 0.67 to 14.7 +/- 0.64, and 6.4 +/- 0.3 to 5.5 +/- 0.4 mg/dl, respectively, P less than 0.004). No significant changes in any of these variables were noticed in the placebo group. Mid-arm circumference and triceps skinfold thickness were measured in 11 carnitine and 13 placebo treated patients. Calculated mid-arm muscle area increased in the carnitine patients (41.37 +/- 2.68 to 45.6 +/- 2.82 cm2, P = 0.05) and remained unchanged in the placebo patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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