Decreased level of serum carnitine might lead to arteriosclerosis progression via the accumulation of advanced glycation end products in maintenance hemodialysis patients

Abstract

Abstract Background Carnitine is reported to improve insulin resistance and reduce oxidative stress. Hyperglycemia and increased oxidative stress are well known to promote the production of advanced glycation end products (AGEs) that can lead to arteriosclerosis in patients with maintenance hemodialysis (HD). In the present study, we aimed to determine whether decreased level of serum carnitine accelerated arteriosclerosis and to clarify the relationships between carnitine, AGEs, and arteriosclerosis in HD patients. Methods We recruited 116 patients (65 men and 51 women, 62 ± 13 years) undergoing HD three times a week. We measured pre-HD serum free carnitine prior to the first weekly session. AGE level was quantitatively evaluated by measuring skin autofluorescence (SAF) with AGE reader. Arteriosclerosis was evaluated by measuring carotid intima-media thickness (cIMT). Relationships between free carnitine, SAF, and cIMT were analyzed, and significant limiting factors for arteriosclerosis were identified using univariate and multivariate regression analyses. Results Free carnitine ranged from 14.9 to 53.3 μmol/L (mean, 28.6 ± 8.1 μmol/L). Free carnitine was negatively correlated with SAF (r = − 0.223, P = 0.017) and cIMT (r = − 0.252, P = 0.006). SAF was positively correlated with cIMT (r = 0.263, P = 0.005). Free carnitine was identified as a significant independent limiting factor for cIMT (β = -0.194, P = 0.037). Conclusions Decreased level of serum carnitine might lead to the progression of arteriosclerosis via the AGE accumulation in HD patients.

Keywords

• Advanced glycation end products
• Arteriosclerosis
• Carnitine
• Hemodialysis