Influence of haemodialysis on early markers of atherosclerosis

End-stage renal disease (ESRD) patients treated by haemodialysis (HD) have impaired endothelium-dependent vasodilatation and increased intima-media thickness (IMT) of the carotid artery The aim of the study was to analyse the relationships between parameters of chronic HD treatment and non-invasive assessments of preclinical atherosclerosis (endothelial dysfunction and carotid IMT) in ESRD patients on HD.

Fifty-two (19 females, 33 males) adult patients on chronic maintenance (4.65 +/- 3.29 years) HD aged 59.88 +/- 15.49 years were investigated. Ultrasonographic studies were performed with a 7.5 MHz high-resolution probe. The common carotid artery IMT was measured. Brachial artery diameter was analysed to the rest. In order to assess flow-mediated dilatation (FMD), hyperaemia was induced by a pneumatic cuff, and an analysis of the diameter was performed 1, 2, 3 and 4 min after cuff deflation.

Significant differences were found in the average carotid IMT value between subjects with delivered dialysis dose (Kt/V) > or =1.2 and <1.2 (0.89 +/- 0.21 vs 1.04 +/- 0.11, P = 0.0045). A correlation between Kt/V and IMT (r = 0.366, P = 0.004) was demonstrated. FMD values of the brachial artery did not correlate with Kt/V. A correlation between low molecular weight heparin per kg of body mass and maximal percent of FMD was demonstrated (r = -0.242, P = 0.049). The maximal percent of brachial FMD was correlated with absolute difference between pre- and postdialysis pulse pressure values (r = -0.265, P = 0.033). In a partial correlation with haemoglobin as control, a variable significant correlation between total erythropoietin dose and maximal carotid IMT (r = -0.262, P = 0.036) was found. In a multiple linear regression model, Kt/V was independently correlated with carotid IMT values (beta = -0.227, P = 0.0335).

This study has demonstrated the association between HD procedure and early atherosclerosis markers. HD treatment has to be considered as potential modifying factor in atherosclerosis development.