Altered expression of serum miR‐106a, miR‐19b, miR‐17, and PTEN in patients with idiopathic membranous nephropathy

BACKGROUND: To find new diagnostic markers for idiopathic membranous nephropathy (IMN) and also conduct preliminary explorations into the possible pathogenesis of IMN by comparing the expression of microRNA‐451a (miR‐451a), miR‐106a, miR‐19b, miR‐17, and phosphatase and tensin homolog (PTEN) protein in the serum of patients with IMN and healthy controls. METHODS: The expression levels of miR‐451a, miR‐106a, miR‐19b, and miR‐17 in the serum of patients in the IMN group (n = 55, age: 50.2 ± 12.1 years) and the control group (n = 58, age 47.4 ± 13.1 years) were measured by quantitative real‐time polymerase chain reaction (qRT‐PCR), and the concentration of serum PTEN protein was determined by enzyme‐linked immunosorbent assay (ELISA). RESULTS: Compared with the control group, the expression of miR‐106a, miR‐19b, and miR‐17 was decreased significantly in the IMN group, whereas PTEN protein concentration was increased significantly in the IMN group. The areas under the receiver operating characteristic curve (AUC) of serum miR‐106a, miR‐19b, miR‐17, and PTEN were 0.66 (95% confidence interval [CI], 0.56–0.76), 0.81 (95% CI, 0.73–0.89), 0.69 (95% CI, 0.59–0.79), and 0.86 (95% CI, 0.79–0.93), respectively. The level of serum PTEN protein was negatively correlated with the expression of miR‐106a and miR‐19b. PTEN concentration was positively correlated with serum urea (Urea), creatinine (Crea), cystatin C (Cysc), 24 h urine total protein (24 h‐UP) and negatively correlated with albumin (Alb) and estimated glomerular filtration rate (eGFR). CONCLUSIONS: MiR‐106a, miR‐19b, miR‐17, and PTEN are involved in the pathogenesis of IMN and may become new biomarkers for the diagnosis of IMN.