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Background <p>Chronic kidney disease (CKD) is a global health challenge accelerated by obesity. This study evaluated the association of peripheral Cluster of Differentiation 36 (CD36) mRNA expression and serum soluble CD36 (sCD36) with CKD, investigating how obesity modulates these markers.</p> Methods <p>Seventy-five participants were stratified into controls (<i>n</i> = 25), non-obese CKD (<i>n</i> = 25), and obese CKD patients (<i>n</i> = 25). Markers were quantified via RT-qPCR and ELISA.</p> Results <p>Both CD36 mRNA and serum sCD36 significantly increased in CKD, peaking in the obese CKD group (<i>p</i> &lt; 0.001). While strongly correlated across the whole cohort (<i>r</i> = 0.69, <i>P</i> &lt; 0.001), stratified analysis revealed divergent behaviors. CD36 mRNA lost lipid associations but selectively correlated with serum urea exclusively in the obese CKD subgroup (<i>r</i> = 0.42, <i>P</i> = 0.04). Conversely, serum sCD36 maintained robust, obesity-independent correlations with pro-atherogenic lipids (triglycerides, total cholesterol, Low-Density Lipoprotein (LDL); <i>P</i> &lt; 0.001) and an inverse correlation with High-Density Lipoprotein (HDL) in both CKD cohorts, losing renal associations. ROC analysis demonstrated superior diagnostic performance for serum sCD36 (Area Under the Curve (AUC) = 0.94, sensitivity 98%, specificity 84% at 0.64 ng/mL) over mRNA expression (AUC = 0.87, sensitivity 82%, specificity 88%) in discriminating CKD from controls.</p> Conclusion <p>CD36 transcriptional and translational tiers exhibit distinct dynamics in CKD. Peripheral mRNA reflects localized uremic stress under obese conditions, whereas circulating sCD36 serves as a stable, obesity-independent indicator of systemic lipotoxicity and a potential diagnostic or associative biomarker.</p>

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Study of CD36 receptor gene expression in obese and non-obese chronic kidney disease patients

  • 期刊论文

  • 发表日期：

    2026年6月30日

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  • Asmaa G Yehia,
  • Nora Seliem,
  • Saad El Deen Mohamed Elsheref,
  • Wafaa Abdelaziz Emam

摘要

Background

Chronic kidney disease (CKD) is a global health challenge accelerated by obesity. This study evaluated the association of peripheral Cluster of Differentiation 36 (CD36) mRNA expression and serum soluble CD36 (sCD36) with CKD, investigating how obesity modulates these markers.

Methods

Seventy-five participants were stratified into controls (n = 25), non-obese CKD (n = 25), and obese CKD patients (n = 25). Markers were quantified via RT-qPCR and ELISA.

Results

Both CD36 mRNA and serum sCD36 significantly increased in CKD, peaking in the obese CKD group (p < 0.001). While strongly correlated across the whole cohort (r = 0.69, P < 0.001), stratified analysis revealed divergent behaviors. CD36 mRNA lost lipid associations but selectively correlated with serum urea exclusively in the obese CKD subgroup (r = 0.42, P = 0.04). Conversely, serum sCD36 maintained robust, obesity-independent correlations with pro-atherogenic lipids (triglycerides, total cholesterol, Low-Density Lipoprotein (LDL); P < 0.001) and an inverse correlation with High-Density Lipoprotein (HDL) in both CKD cohorts, losing renal associations. ROC analysis demonstrated superior diagnostic performance for serum sCD36 (Area Under the Curve (AUC) = 0.94, sensitivity 98%, specificity 84% at 0.64 ng/mL) over mRNA expression (AUC = 0.87, sensitivity 82%, specificity 88%) in discriminating CKD from controls.

Conclusion

CD36 transcriptional and translational tiers exhibit distinct dynamics in CKD. Peripheral mRNA reflects localized uremic stress under obese conditions, whereas circulating sCD36 serves as a stable, obesity-independent indicator of systemic lipotoxicity and a potential diagnostic or associative biomarker.