Circulating CD5L is associated with cardiovascular events and all-cause mortality in individuals with chronic kidney disease

Abstract

This study assessed the association of CD5L and soluble CD36 (sCD36) with the risk of a cardiovascular event (CVE), including CV death and all-cause mortality in CKD. We evaluated the association of CD5L and sCD36 with a predefined composite CV endpoint (unstable angina, myocardial infarction, transient ischemic attack, cerebrovascular accident, congestive heart failure, arrhythmia, peripheral arterial disease [PAD] or amputation by PAD, aortic aneurysm, or death from CV causes) and all-cause mortality using Cox proportional hazards regression, adjusted for CV risk factors. The analysis included 1,516 participants free from pre-existing CV disease followed up for 4 years. The median age was 62 years, 38.8% were female, and 26.8% had diabetes. There were 98 (6.5%) CVEs and 72 (4.8%) deaths, of which 26 (36.1%) were of CV origin. Higher baseline CD5L concentration was associated with increased risk of CVE (HR, 95% CI, 1.17, 1.0–1.36), and all-cause mortality (1.22, 1.01–1.48) after adjusting for age, sex, diabetes, systolic blood pressure, dyslipidemia, waist circumference, smoking, and CKD stage. sCD36 showed no association with adverse CV outcomes or mortality. Our study showed for the first time that higher concentrations of CD5L are associated with future CVE and all-cause mortality in individuals with CKD.

Scavenger Receptors in Myocardial Infarction and Ischemia/Reperfusion Injury: The Potential for Disease Evaluation and Therapy

“…However, in another study in which 1516 participants with chronic kidney disease were followed for 4 years, plasma concentrations of sCD36 were not associated with an increased risk of the defined or predefined composite cardiovascular end point and all‐cause mortality. 20 However, increased plasma concentrations of CD5 L could be a predictor of an increased risk of cardiovascular events in these patients. Overall, sCD36 may be a predictive or diagnostic marker for patients with MI, although further clinical studies are necessary in the future (Table 2 ).…”

“…Along with the transport of HDL, SR‐BI can promote the clearance of LDL, very LDL, and apolipoprotein A, contributing to the attenuation of atherosclerosis. 20 CD36 (a gene located on chromosome 7 of humans) is expressed on macrophages, monocytes, ECs, SMCs, platelets, and cardiac myocytes (Figure 1 ; Table 1 ) and has been reported to play an important role in inflammation, angiogenesis, and atherosclerosis by binding different ligands. 21 In macrophages, oxLDL can increase CD36 expression, and CD36 recognizes and facilitates the endocytosis of oxLDL, resulting in the development of foam cells and the progression of atherosclerosis.…”

The serum soluble scavenger with 5 domains levels: A novel biomarker for individuals with heart failure

“…Agra-Bermejo et al suggested that isoproterenol treatment of patients with HF or atrial fibrillation significantly increased CD5L secretion from epicardial adipose tissue, which may activate the toll-like receptor 4/nuclear factor-kappa B (NF-κB) signaling pathway and produce pro-inflammatory cytokines ( Agra-Bermejo et al, 2020 ). Circulating CD5L is highly correlated with the risk of cardiovascular events in patients with chronic kidney dysfunction ( Castelblanco et al, 2021 ). Moreover, CD5L promotes atherosclerosis by increasing the formation of macrophage foam cells and CD36-mediated oxidized low-density lipoprotein uptake ( Amézaga et al, 2014 ).…”

Identification of biomarkers and pathways for focal segmental glomerulosclerosis using next generation sequencing data and bioinformatics analysis

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