Expression of Scavenger Receptor CD36 in Chronic Renal Failure Patients

Chmielewski, Michael S.; Bryl, Ewa; Marzec, Lukasz; Aleksandrowicz, Ewa; Witkowski, Jacek M.; Rutkowski, Bolesław

doi:10.1111/j.1525-1594.2005.29097.x

Cited by 46 publications

(26 citation statements)

References 26 publications

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“…Interestingly, numerous studies have suggested enhanced scavenger receptor expression on cells of the monocyte/macrophage lineage, along with defects in macrophage cholesterol efflux, in humans with CKD. [29][30][31][32][33] Furthermore, studies in ApoE 2/2 mice, a rodent model of atherosclerosis, demonstrate that induction of kidney disease in this model enhances macrophage cholesterol accumulation independent of alterations in plasma cholesterol concentrations. 34 This investigation has both important strengths and limitations.…”

Section: Discussionmentioning

confidence: 99%

Serum Trimethylamine-N-Oxide is Elevated in CKD and Correlates with Coronary Atherosclerosis Burden

Stubbs

House

Ocque

et al. 2016

Journal of the American Society of Nephrology

343

334

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Trimethlyamine-N-oxide (TMAO) was recently identified as a promoter of atherosclerosis. Patients with CKD exhibit accelerated development of atherosclerosis; however, no studies have explored the relationship between TMAO and atherosclerosis formation in this group. This study measured serum concentrations and urinary excretion of TMAO in a CKD cohort (n=104), identified the effect of renal transplant on serum TMAO concentration in a subset of these patients (n=6), and explored the cross-sectional relationship between serum TMAO and coronary atherosclerosis burden in a separate CKD cohort (n=220) undergoing coronary angiography. Additional exploratory analyses examined the relationship between baseline serum TMAO and long-term survival after coronary angiography. Serum TMAO concentrations demonstrated a strong inverse association with eGFR (r 2 =0.31, P,0.001). TMAO concentrations were markedly higher in patients receiving dialysis (median [interquartile range], 94.4 mM [54.8-133.0 mM] for dialysis-dependent patients versus 3.3 mM [3.1-6.0 mM] for healthy controls; P,0.001); whereas renal transplantation resulted in substantial reductions in TMAO concentrations (median [min-max] 71.2 mM [29.2-189.7 mM] pretransplant versus 11.4 mM [8.9-20.2 mM] posttransplant; P=0.03). TMAO concentration was an independent predictor for coronary atherosclerosis burden (P=0.02) and predicted long-term mortality independent of traditional cardiac risk factors (hazard ratio, 1.26 per 10 mM increment in TMAO concentration; 95% confidence interval, 1.13 to 1.40; P,0.001). In conclusion, serum TMAO concentrations substantially increase with decrements in kidney function, and this effect is reversed by renal transplantation. Increased TMAO concentrations correlate with coronary atherosclerosis burden and may associate with long-term mortality in patients with CKD undergoing coronary angiography. Patients with CKD have a high prevalence of cardiovascular comorbidities, which primarily contributes to the exceedingly high mortality in this group. 1,2 For example, the 5-year survival for ESRD patients receiving dialysis is approximately 35%, with .50% of the mortality in this group resulting directly from cardiovascular causes. 1 It is well established that CKD patients exhibit a disproportionate burden of atherosclerosis as compared with individuals having normal kidney function. [2][3][4][5] Furthermore, a higher prevalence of traditional risk factors for the development of atherosclerosis, such as hypertension, diabetes and hyperlipidemia, only partially accounts for the accelerated atherosclerosis in CKD patients, leading to the hypothesis that unique risk factors must be present in this population. 6,7

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Section: Discussionmentioning

confidence: 99%

Serum Trimethylamine-N-Oxide is Elevated in CKD and Correlates with Coronary Atherosclerosis Burden

Stubbs

House

Ocque

et al. 2016

Journal of the American Society of Nephrology

343

334

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“…Monocytes in patients with chronic renal failure (CRF), who are at high risk of atherothrombosis, showed by flow cytometry much higher CD36 expression levels following peritoneal dialysis or hemodialysis compared to controls with no renal impairment. Statin treatment of such patient's significantly reduced the CD36 expression level which is strongly associated with enhanced risk of atherothrombosis [57]. It is interesting to note that statins not only affected CD36 expression in monocytes/macrophages but also in circulating platelets.…”

Section: Statins and Plaque Stabilitymentioning

confidence: 99%

Statin Therapy-Evidence Beyond Lipid Lowering Contributing to Plaque Stability

Lorenzo¹,

Feher²,

Martin³

et al. 2006

CMC

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Primarily statin drugs inhibit hepatic 3-hydroxy 3-methylglutaryl coenzyme A (HMG-CoA) reductase, which is responsible for the reduction in circulating low-density lipoprotein (LDL) cholesterol. Several findings from recent research studies indicate that statins have multiple actions that favorably influence key factors involved in the atherogenic process. These so-called pleiotropic properties affect various aspects of cell function, inflammation, coagulation, and vasomotor activity. These effects are mediated either indirectly through LDL cholesterol reduction or via a direct effect on cellular functions. Such actions may contribute to the early cardiovascular benefit observed in several outcome trials with statin drugs therapy. Although many of the pleiotropic properties of statins may be a class effect, some may be unique to certain agents and account for differences in their pharmacological activity. This review summarise the results of the major outcome trials of statins and non-statins therapy and the possible mechanisms beyond lipid lowering contributing to plaque stability.

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“…14 -16 Peripheral blood monocyte CD36 levels are significantly higher in patients on dialysis than in normal individuals. 17 In a recent study, we demonstrated the kidneys of mice with diet-induced hypercholesterolemia developed worse fibrosis after unilateral ureteral obstruction (UUO) than did normocholesterolemic mice. This difference was associated with higher renal oxidized lipoprotein levels, activation of inflammatory pathways, and a striking change in the intensity and cell-specific pattern of CD36 expression.…”

mentioning

confidence: 99%

CD36 Regulates Oxidative Stress and Inflammation in Hypercholesterolemic CKD

Okamura

Pennathur

Pasichnyk

et al. 2009

Journal of the American Society of Nephrology

127

119

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Scavenger receptors play a central role in atherosclerosis by processing oxidized lipoproteins and mediating their cellular effects. Recent studies suggested that the atherogenic state correlates with progression of chronic kidney disease (CKD); therefore, scavenger receptors are candidate mediators of renal fibrogenesis. Here, we investigated the role of CD36, a class B scavenger receptor, in a hypercholesterolemic model of CKD. We placed CD36-deficient mice and wild-type male mice on a high-fat Western diet for 7 to 8 wk and then performed either sham or unilateral ureteral obstruction surgery. CD36-deficient mice developed significantly less fibrosis compared with wild-type mice at days 3, 7, and 14 after obstruction. Compared with wild-type mice, CD36-deficient mice had significantly more interstitial macrophages at 7 d but not at 14 d. CD36-deficient mice exhibited reduced levels of activated NF-B and oxidative stress (assessed by measuring fatty acid-derived hydroxyoctadecadienoic acid and protein carbonyl content) and decreased accumulation of interstitial myofibroblasts compared with wild-type mice. These data suggest that CD36 is a key modulator of proinflammatory and oxidative pathways that promote fibrogenesis in CKD.

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Expression of Scavenger Receptor CD36 in Chronic Renal Failure Patients

Abstract: 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.

Cited by 46 publications

References 26 publications

Serum Trimethylamine-N-Oxide is Elevated in CKD and Correlates with Coronary Atherosclerosis Burden

Serum Trimethylamine-N-Oxide is Elevated in CKD and Correlates with Coronary Atherosclerosis Burden

Statin Therapy-Evidence Beyond Lipid Lowering Contributing to Plaque Stability

CD36 Regulates Oxidative Stress and Inflammation in Hypercholesterolemic CKD

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