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Stage-dependent alterations in MaR1 in pediatric chronic kidney disease: a potential candidate biomarker
Muhammet Akif Guler1, Muhammet Celik2, Hamza Halici3
1Department of Pediatric Nephrology, State Hospital, Erzurum, 25240, Turkey.
Background:
Chronic kidney disease (CKD) in children is characterized by persistent inflammation and oxidative stress, contributing to progressive loss of renal function and multisystem involvement. Maresin 1 (MaR1), a specialized pro-resolving lipid mediator derived from docosahexaenoic acid (DHA), plays a role in the resolution of inflammation and tissue repair. However, its circulating concentrations in pediatric CKD have not been examined. This study aimed to determine serum MaR1 levels across CKD stages in children and to assess its potential relevance as a biomarker reflecting disease severity.
Methods:
Children were categorized as healthy controls or assigned to CKD stages 1-5 according to estimated glomerular filtration rate (eGFR). In patients receiving hemodialysis, blood samples were obtained 48 h after the preceding dialysis session and immediately before the subsequent session. Serum MaR1 concentrations were measured by enzyme-linked immunosorbent assay (ELISA). Group comparisons were performed using one-way ANOVA with Tukey's post-hoc test (p < 0.05).
Results:
Serum MaR1 levels differed significantly among the six groups (p < 0.001). Mean MaR1 concentrations were 110.20 ± 18.15 pg/mL in healthy controls, 20.01 ± 7.23 pg/mL in CKD stage 1, 39.61 ± 7.60 pg/mL in stage 2, 60.73 ± 12.79 pg/mL in stage 3, 203.86 ± 22.06 pg/mL in stage 4, and 284.56 ± 25.75 pg/mL in stage 5. MaR1 levels showed a marked reduction at stage 1, followed by progressive recovery and substantial elevation in advanced CKD.
Conclusions:
Serum MaR1 concentrations show a stage-dependent pattern in pediatric CKD, characterized by marked suppression at stage 1 followed by progressive recovery and elevation in advanced stages. These findings suggest that circulating MaR1 may represent a candidate biomarker of disease-related inflammatory dynamics; however, its clinical utility requires validation in larger longitudinal studies.
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