Cardiovascular complications in CKD 5d

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Introduction and Aims: CD36 is a member of a class of cell surface glycoproteins designated as type B scavenger receptors. A ligand for receptor CD36 is oxidized low density lipoprotein (OxLDL). CD36 binds and internalizes OxLDL and is reported as a player in the development of atherosclerosis. Recently salusin-alpha is indicated as an endogenous inhibitor of atherosclerosis. Experimental data on salusin-alpha influence on CD36 expression are controversial. The aim of our study was to examine a correlation between serum salusin-alpha level and CD36 count and expression in intermittent hemodialysis (IHD) patients treated due to abnormal serum lipid profile with low fat-diet and planned physical activity. Methods: A cross-sectional analysis was performed in 45 IHD patients maintained on low fat-diet and planned physical activity through 8 weeks. The group included 14 persons with coronary artery disease (CAD); 9 of them had history of myocardial infarction. The level of expression of CD36 on peripheral blood monocytes was evaluated by flow cytometric analysis, using APC Mouse Anti-Human CD36 (BD Pharmingen, USA) and a mixture of fluorescein isothiocyanate-conjugated anti-CD45 and phycoerythrin-conjugated anti-CD14 (Simultest™ LeucoGATE™, USA) for white cell differentiation. Monocytes were gated selectively for analysis by low-forward-angle light scatter and right-angled light scatter. Serum levels of salusin-alpha, total cholesterol (Ch), high density lipoprotein (HDL)-Ch and triacylglycerols were simultaneously determined. Radioimmunoassay method (Phoenix Pharmaceuticals, USA) was applied for salusin-alpha measurement. Results: In all IHD patients serum salusin-alpha concentration was 15.5 ± 7.0 pmol/L, CD36 count 375 ± 164 cells/mL, and mean fluorescence intensity (MFI) 1,419 ± 862. Serum lipids were as follows: total Ch 205 ± 41 mg/dL, HDL-Ch 43.5 ± 9.2 mg/dL, triacylglycerols 209 ± 103 mg/dL. Respective results of these parameters did not differ significantly between CAD and non-CAD patients. Serum salusin-alpha correlated with CD36 expression (MFI) in all patients (r = 0.384, p = 0.009) and in non-CAD group (r = 0.443, p = 0.013). In CAD patients a correlation between salusin-alpha and CD36 count was shown (r = 0.695, p = 0.006), whereas a correlation with CD36 expression did not reach statistical significance (r = 0.389). Additionally, in CAD group salusin-alpha negatively correlated with HDL-Ch (r = -0.526, p = 0.005). Conclusions: If according to the current data salusin-alpha is an inhibitor of atherosclerosis, whereas CD36 promotes atherosclerosis, the explanation of our results is that in hyperlipidemic IHD patients serum salusin-alpha may exert a protective action against atherosclerosis in response to higher CD36 expression/count and lower HDL-cholesterol. (ClinicalTrials.gov number, NCT01448174)

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