Abstract
L-carnitine (LC) supplementation improves cardiac function in hemodialysis (HD) patients. However, whether reducing LC supplementation affects carnitine kinetics and cardiac function in HD patients treated with LC remains unclear. Fifty-nine HD patients previously treated with intravenous LC 1000 mg per HD session (three times weekly) were allocated to three groups: LC injection three times weekly, once weekly, and placebo, and prospectively followed up for six months. Carnitine fractions were assessed by enzyme cycling methods. Plasma and red blood cell (RBC) acylcarnitines were profiled using tandem mass spectrometry. Cardiac function was evaluated using echocardiography and plasma B-type natriuretic peptide (BNP) levels. Reducing LC administration to once weekly significantly decreased plasma carnitine fractions and RBC-free carnitine levels during the study period, which were further decreased in the placebo group (p < 0.001). Plasma BNP levels were significantly elevated in the placebo group (p = 0.03). Furthermore, changes in RBC (C16 + C18:1)/C2 acylcarnitine ratio were positively correlated with changes in plasma BNP levels (β = 0.389, p = 0.005). Reducing LC administration for six months significantly decreased both plasma and RBC carnitine levels, while the full termination of LC increased plasma BNP levels; however, it did not influence cardiac function in HD patients.
Highlights
Heart failure (HF), as well as some of its complications, such as pulmonary edema, is a serious condition characterized by decreased myocardial contractility and abnormal hemodynamic state in patients with end-stage kidney disease (ESKD)
Two patients were excluded from the study because red blood cell (RBC) acylcarnitine levels were not measured
A total of 51 patients completed the treatment in the groups: LC 3 Times/w (LC-3) group (n = 18), LC-1 group (n = 16), and LC-3; p < 0.01; three times weekly (LC-0) group (n = 17) (Figure 1)
Summary
Heart failure (HF), as well as some of its complications, such as pulmonary edema, is a serious condition characterized by decreased myocardial contractility and abnormal hemodynamic state in patients with end-stage kidney disease (ESKD). Renal Data System revealed that an estimated 44% of patients on hemodialysis (HD) have chronic HF (CHF), and 5.4% of HD patients die of chronic HF [1] Transplantation has reported that HF is the most common cause of death in patients undergoing dialysis [2]. CHF is associated with impairments in activities of daily living and quality of life in HD patients [3]. The prevention of HF development is a crucial therapeutic strategy for HD patients worldwide
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