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Expression of scavenger receptor CD36 in chronic renal failure patients
Michal Chmielewski1, Ewa Bryl, Lukasz Marzec
1Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland. chmiel@amg.gda.pl
Insights
Patients with chronic renal failure (CRF) show higher expression of the scavenger receptor CD36 on monocytes, a potential risk factor for atherosclerosis. Statin therapy was associated with reduced CD36 expression in these patients.
Area of Science:
- Nephrology
- Cardiology
- Immunology
Background:
- Chronic renal failure (CRF) patients face elevated atherosclerosis risk.
- Foam cell formation is a key step in atherosclerosis pathogenesis.
- Scavenger receptor CD36 mediates oxidized low-density lipoprotein uptake, crucial for foam cell formation.
Purpose of the Study:
- To investigate CD36 scavenger receptor expression on blood monocytes in CRF patients.
- To assess the relationship between CD36 expression and renal replacement therapy modalities.
- To evaluate the impact of statin treatment on CD36 expression in CRF.
Main Methods:
- Flow cytometry was used to measure CD36 expression on monocytes from hemodialysis (HD), peritoneal dialysis (PD), predialysis, and control groups.
- Lipid peroxidation markers, malondialdehyde (MDA) and 4-hydroxyalkenals (HAE), were quantified.
- The effect of statin therapy on CD36 expression was analyzed.
Main Results:
- Monocyte CD36 expression was significantly higher in HD and PD patients compared to controls.
- Predialysis patients did not show significantly higher CD36 expression than controls.
- Elevated MDA and HAE levels were found in all CRF subgroups; statin users had lower CD36 expression.
Conclusions:
- This study is the first to report increased CD36 scavenger receptor expression in CRF patients.
- Elevated CD36 expression may contribute to accelerated atherogenesis in CRF.
- Statin therapy may mitigate CD36-related atherosclerosis risk in CRF patients.
Background:
Patients with chronic renal failure (CRF) are at increased risk of atherosclerosis development. One of the major steps in pathogenesis of atherosclerosis is formation of foam cells. Scavenger receptor CD36 is among the major receptors for oxidized low density lipoproteins (oxLDL) and therefore it plays a crucial role in foam cell formation. The aim of the present study was to investigate the expression of CD36 on blood monocytes of CRF patients.
Methods:
Expression of CD36 on blood monocytes of CRF patients treated with hemodialysis (HD), peritoneal dialysis (PD), those not yet on dialysis (predialysis), and controls was assessed with the use of flow cytometry. Additionally, the major lipid peroxidation markers, malondialdehyde (MDA) and 4-hydroxyalkenals (HAE), were measured. Further, impact of treatment with HMG-CoA reductase inhibitors (statins) on CD36 expression in CRF patients was evaluated.
Results:
Expression of monocyte CD36, measured as mean fluorescence intensity (MFI) was significantly higher in HD and PD patients, when compared to controls without renal insufficiency (respectively: 1011 +/- 288 and 1000 +/- 309 vs. 710 +/- 313; P < 0.01 for both groups). This was not the case in predialysis group (828 +/- 363 vs. 710 +/- 313). Higher concentrations of lipid peroxidation indicators, MDA and HAE were observed in all three subgroups of CRF patients (2.1 +/- 0.51, 2.02 +/- 0.27, and 1.81 +/- 0.53 microm in HD, PD, and predialysis group, respectively, vs. 1.13 +/- 0.59 microm in controls; P < 0.01). Patients treated with statins showed significantly lower CD36 expression than patients without statin therapy.
Conclusions:
The present study, for the first time, demonstrates increased expression of CD36 scavenger receptor in CRF patients. This may be a possible risk factor for accelerated atherogenesis observed in this group of patients.
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