Abstract Background and Aims The development of new pathogenetic treatment programs to reduce cardiovascular risk in diabetic patients with end-stage kidney disease is an important task of modern nephrology. In these conditions, considering the essential role of magnesium and L-carnitine deficiency in the mechanisms (via endothelial and metabolic disorders) of cardiovascular diseases, we evaluated the effect of the combined use of magnesium aspartate and L-carnitine on inflammation, insulin resistance and the atherosclerosis progression of carotid arteries in type 2 diabetic hemodialysis (HD) patients. Method 42 type 2 diabetic HD patients were included in this prospective cohort study (male, 26; age, 59.5 ± 0.7 years; HD duration, 31.2 ± 4.6 month; diabetes mellitus duration, 174.6 ± 7.8 month). Depending on the treatment programme, patients were divided into two groups: the 1st (main) group (n = 22) in addition to basic treatment (hypoglycemic, antihypertensive therapy, correction of anemia, hyperparathyroidism, hyperphosphatemia) was treated by combination of magnesium aspartate (0.5 g/day orally) and L-carnitine (1 g/day parenterally after each HD session (three times weekly); the 2nd (comparison) group (n = 20) was only on the standard therapy. Complex treatment lasted 12-months; administration of L-carnitine was performed continuously throughout the year, while magnesium aspartate – by three 2-months’ courses per year. Serum content of tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP) and fibrinogen as inflammatory biomarkers were determined. The homoeostasis model of assessment-insulin resistance (HOMA-IR) as an index of insulin resistance was estimated. Common carotid artery intima-media thickness (CСА IMT) as an index of the atherosclerosis severity was measured by ultrasound. Data are expressed as means ± SEM. Wilcoxon T-test was used for comparison of the dependent variables, Mann-Whitney U-test – for independent ones. Results In diabetic HD patients undergoing complex treatment with a combination of magnesium aspartate and L-carnitine after 12 months of observation CCA IMT did not change (0.88 ± 0.05 vs. 0.88 ± 0.05 mm; Z = 0.09, p = 0.925), while a significant increase (by 9.1%) in the CCA IMT was determined in subjects, who were on basic therapy (0.98 ± 0.04 vs. 1.07 ± 0.04 mm; Z = 2.27, p = 0.023). In addition, after 12 months of treatment, the indicated index between 1st and 2nd groups differed (p = 0.006). By the end of follow-up, the TNF-α, CRP and fibrinogen contents in patients who were on modified therapy were 44.7, 56.4 and 78.2% from baseline, a similar indices in patients receiving standard treatment – 70.7, 77.3 and 88.8% respectively, and after one year the main group and the comparison group on the serum concentrations of TNF-α (p = 0.089), CRP (p = 0.030) and fibrinogen (p = 0.026) differed. Magnesium aspartate and L-carnitine supplementation significantly improve HOMA-IR, and after 12 months of observation, the indicated index in the 2nd group exceeded (p = 0.003) that in the 1st one (Table 1). Conclusion (1) The combined use of magnesium aspartate and L-carnitine, in addition to the basic 12-month treatment, prevents the atherosclerosis progression of CCA, provides an effective reduction of the activity of chronic inflammation, improves insulin resistance in type 2 diabetic HD patients. (2) Long-term modified treatment may reduce the cardiovascular risk in these subjects.
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