Changes of serum Mir-217 and the correlation with the severity in type 2 diabetes patients with different stages of diabetic kidney disease

The aim of this study is to investigate the correlation between serum microRNA-217 and the severity of diabetic kidney disease determined by albuminuria. Four hundred ninety five type 2 diabetes patients were divided into three groups: normoalbuminuric group, microalbuminuric group, and macroalbuminuric group. Serum microRNA-217 levels were validated by real-time polymerase chain reaction. Serum silent information regulator 1, Hypoxia-inducible factor-1 alpha and vascular endothelial growth factor were determined by enzyme-linked immunosorbent assay. Compared with control, serum microRNA-217 levels were significantly increased in type 2 diabetes patients and gradually increased in patients of normoalbuminuric, microalbuminuric, and macroalbuminuric groups (P < 0.01). Moreover, increased levels of serum microRNA-217, hypoxia-inducible factor-1 alpha, vascular endothelial growth factor, diabetes mellitus duration, fasting blood glucose, fasting insulin, homeostasis model assessment for insulin resistance, glycated hemoglobin, low-density lipoprotein, total cholesterol, triglyceride, uric acid, serum creatinine, blood urea nitrogen, and decreased levels of serum silent information regulator 1 and high-density lipoprotein were significantly correlated with Ln(ACR) (P < 0.05). In addition, serum microRNA-217 was positively correlated with diabetes mellitus duration, homeostasis model assessment for insulin resistance, glycated hemoglobin, Ln(ACR), low-density lipoprotein, total cholesterol, triglyceride, uric acid, serum creatinine, blood urea nitrogen, hypoxia-inducible factor-1 alpha, vascular endothelial growth factor (P < 0.05), and negatively correlated with serum silent information regulator 1 (P = 0.002). Our findings suggest that microRNA-217 may have an association with the development of proteinuria in type 2 diabetes patients. Serum microRNA-217 may be involved in the development of diabetic kidney disease by promoting chronic inflammation, renal fibrosis, and angiogenesis.