Urinary N-acetyl-ß-d-glucosaminidase-creatine ratio is a valuable predictor for advanced diabetic kidney disease.

BACKGROUND: Many biomarkers show high diagnostic values for diabetic kidney disease (DKD), but fewer studies focus on the predictive assessment of DKD progression by blood and urinary biomarkers. AIM: This study aims to find powerful risk predictors and identifying biomarkers in blood and urine for DKD progression. METHODS: A total of 117 patients with type 2 DKD including early and advanced stages and their laboratory parameters were statistically assessed. A receiver operating characteristic (ROC) curve analysis was performed to evaluate the significance of discriminating between early and advanced DKD, and the predictive power for advanced DKD was analyzed by regression analysis and trisector grouping. RESULTS: N-acetyl-ß-d-glucosaminidase-creatine (NAG/CR) level in advanced DKD was statistically higher than that in early DKD (p < 0.05), and there was a higher incidence of advanced DKD (72% vs. 56%) and high odds ratio (OR: 3.917, 95% CI: 1.579-10.011) of NAG/CR with ≥2.79 U/mmol compared with <2.79 U/mmol (p < 0.05). NAG/CR ratio also showed a higher area under the ROC curve of 0.727 (95% CI: 0.616-0.828, p = 0.010) with a high sensitivity (0.75) and a moderate specificity (0.66) when 1.93 U/mmol was set as the optimal cutoff value. The adjusted-multivariable analysis revealed that NAG/CR had an OR of 1.021 (95% CI: 1.024-1.038) and 2.223 (95% CI: 1.231-4.463) based on a continuous and categorical variable, respectively, for risk of advanced DKD. Moreover, the prevalence of advanced DKD exhibited an increasing tendency by an increment of the trisector of NAG/CR. CONCLUSIONS: This study suggests that NAG/CR ratio is an independent predictor for advanced DKD, and it also can be used as a powerful identifying marker between early and advanced DKD.

Myocardial Infarction-Related Transcripts (MIAT) Participate in Diabetic Optic Nerve Injury by Regulating Heart Shock Protein 5 (HSPA5) via Competitively Binding to MicroRNA-379.

BACKGROUND The aim of this study was to explore the role of MIAT (myocardial infarction related transcripts) in diabetic optic neuropathy and its underlying mechanism. MATERIAL AND METHODS QRT-PCR (quantitative real-time polymerase chain reaction) was performed to detect the mRNA levels of MIAT and HSPA5 (heart shock protein 5) in diabetic rat model and high-glucose cultured Müller cells. After the intracellular MIAT level was increased by lentivirus transfection, the proliferation, cell cycle, and apoptosis of Müller cells were measured using the CCK-8 (Cell Counting Kit-8) assay, flow cytometry, and TUNEL (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling) assay, respectively. Mechanisms underlying the MIAT-related apoptosis were explored by Western blot analysis. The binding condition of microRNA-379 to MIAT and HSPA5 was confirmed by luciferase reporter gene assay. RESULTS Both MIAT and HSPA5 levels were remarkably increased in high-glucose cultured Müller cells. After transfected with LV (lentivirus)-MIAT, Müller cells showed a decreased proliferation and an enhanced apoptosis with the increased expressions of pro-apoptotic proteins. However, no remarkable changes were observed in cell cycle. Further mechanistic studies found that MIAT regulated HSPA5 expression by directly binding to microRNA-379. CONCLUSIONS MIAT was overexpressed in the diabetic optic nerve. MIAT overexpression remarkably promoted the apoptosis of Müller cells by adsorbing microRNA-379 and thus regulating HSPA5, which was a direct target of microRNA-379.