Netrin‐1 and clusterin: Innovative potential diagnostic biomarkers for early renal damage in β‐thalassemia major children

Abstract

Background Children with β‐thalassemia major (β‐TM) suffer from tubular dysfunction even before the onset of any renal impairment symptoms and/or clinical signs. Therefore, identifying innovative biomarkers allowing early renal damage detection has focused attention. Aim This study aims to preliminary assess Netrin‐1(NTN‐1) and clusterin (CLU) in β‐TM children and explore their possible roles as surrogate noninvasive biomarkers of renal tubular dysfunction. Subjects and methods In this study, 40 β‐TM children and 30 healthy children were enrolled. Routine serum and urinary biochemical variables were determined. Urinary NTN‐1 and CLU levels were measured using ELISA and their mRNA expression in PBMCs were assayed using real‐time PCR. Serum TNF‐α, MDA levels and GST activity were measured. Results Urinary NTN‐1 and CLU concentrations and mRNA relative expression levels in PBMCs were significantly increased in β‐TM children relative to controls. Oxidative stress and inflammatory markers revealed significant elevation in β‐TM children compared to controls. The change in these parameters correlated significantly with other renal parameters. ROC curves analysis showed that urinary NTN‐1 and CLU levels are of promising diagnostic performance. Conclusion Our results suggest that NTN‐1 and CLU are qualified as new noninvasive biomarker panels for early detection of renal injury in β‐TM children. Moreover, urinary NTN‐1 is recommended as a precise one during the clinical practices.

Differential proteomic patterns of plasma extracellular vesicles show potential to discriminate β-thalassemia subtypes

“…In addition, the urinary levels of CLU are a promising biomarker for kidney injury and early renal damage associated with β-thalassemia in children. 38 IGHG4 lies within a conserved region of the immunoglobulin heavy chains, mediating the effector phase of humoral immunity and helping to eliminate bound antigens. Based on our findings, the differences in immunity abnormalities should drive the subtyping of β-thalassemia patients.…”