Abstract

Introduction and purpose: It is important today to develop new pathogenetic strategies to reduce cardiovascular risk in type 2 diabetic patients with end-stage kidney disease (ESKD). The purpose of the study was to evaluate the efficacy of combine use of magnesium aspartate and L-Carnitine on character of heart changes in dynamics of complex treatment of the patients with diabetic kidney disease (DKD) undergoing hemodialysis (HD). Material and methods: 42 type 2 diabetic ESKD patients were included in this prospective cohort study (male/female, 26/16; age, 59.5±0.7 years; HD duration, 31.2±4.6 months; diabetes mellitus duration, 174,6±7,8 months). The patients were divided into two groups: the 1st (main) group (n=22) was treated by combination of magnesium aspartate (0.5 g/day orally) by three 2-months’ courses/year and L-carnitine (1 g/day parenterally after each HD session) throughout the year; the 2nd (comparison) group (n=20) was only on the basic therapy. The observation time was 12 months. A complete echocardiography and ultrasound scanning of common carotid arteries (CCA) were performed. Results: During follow up period we found the reduction of the left atrium (p=0.008) and left ventricle (LV) diameters (p=0.004), decrease of LV mass index for 17,1% (p=0.005) and prevalence of pseudonormal and restrictive types of LV diastolic dysfunction for 53.3% (p=0.026), increase of the LV ejection fraction for 5.4% (p=0.004), and decrease the mean pulmonary artery pressure for 13% (p=0.009) in the main group. The annual incidence of both mitral and aortic valve calcification in the 2nd group was 10%, in the 1st group – 0%. After 12 months of treatment, increase of the CCA intima-media thickness (p=0.23) was recorded in the comparison group only. Conclusions: The combine use of magnesium and L-carnitine as part of a 12-month complex therapy provides an effective reduction ofLV hypertrophy, improves its systolic and diastolic function, reduces pulmonary hypertension, and prevents the progression of cardiac valve calcification and atherosclerotic damage.

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