E-cadherin as a surrogate marker of epithelial-to-mesenchymal transition for detection of diabetic nephropathy and subclinical atherosclerosis among children and adolescents with type 1 diabete

Background: Epithelial-to-mesenchymal transition (EMT) may be involved in the pathogenesis of diabetic nephropathy (DN) among adults with type 2 diabetes. The current study aimed to evaluate the role of E-cadherin as a surrogate marker of EMT among children and adolescent with type 1 diabetes (T1D) and DN and its possible relation to carotid intima media thickness (CIMT). Research design and methods: Sixty participants with T1D were divided equally into two groups based on urinary albumin creatinine ratio (UACR) and compared with 30 healthy controls. Hemoglobin A1c (HbA1c), kidney function tests, serum E-cadherin and CIMT were assessed. Results: E-cadherin levels were significantly lower in patients with microalbuminuria (56.5 +/- 15.8 ng/mL) compared with patients with normoalbuminuria (179.8 +/- 45.1 ng/mL) and healthy controls (222.5 +/- 39.9 ng/mL) (p < 0.001). E-cadherin correlated negatively with HbA1c (r = -0.42, p = 0.001), UACR (r = -0.89, p < 0.001) and CIMT (r = -0.716, p < 0.001). ROC curve analysis showed that the E-cadherin cutoff value 135 ng/mL could detect nephropathy with 96.67% sensitivity and 86.67% specificity. Logistic regression showed that E-cadherin was a significant independent factor for nephropathy. Conclusions: E-cadherin is a potential biomarker reflecting EMT activity in both pathogenesis and progression of DN and subclinical atherosclerosis in pediatric patients with T1D.