Identifying patients at high risk of diabetic kidney disease (DKD) helps improve clinical outcome. PURPOSETo establish a model for predicting DKD. DATA SOURCESThe derivation cohort was from a meta-analysis. The validation cohort was from a Chinese cohort. STUDY SELECTIONCohort studies that reported risk factors of DKD with their corresponding risk ratios (RRs) in patients with type 2 diabetes were selected. All patients had estimated glomerular filtration rate (eGFR) ‡60 mL/min/1.73 m 2 and urinary albumin-tocreatinine ratio (UACR) <30 mg/g at baseline. DATA EXTRACTIONRisk factors and their corresponding RRs were extracted. Only risk factors with statistical significance were included in our DKD risk prediction model. DATA SYNTHESISTwenty cohorts including 41,271 patients with type 2 diabetes were included in our meta-analysis. Age, BMI, smoking, diabetic retinopathy, hemoglobin A 1c , systolic blood pressure, HDL cholesterol, triglycerides, UACR, and eGFR were statistically significant. All these risk factors were included in the model except eGFR because of the significant heterogeneity among studies. All risk factors were scored according to their weightings, and the highest score was 37.0. The model was validated in an external cohort with a median follow-up of 2.9 years. A cutoff value of 16 was selected with a sensitivity of 0.847 and a specificity of 0.677. LIMITATIONSThere was huge heterogeneity among studies involving eGFR. More evidence is needed to power it as a risk factor of DKD. CONCLUSIONSThe DKD risk prediction model consisting of nine risk factors established in this study is a simple tool for detecting patients at high risk of DKD.

Background: The aim of this study was to evaluate the diagnostic value of six urinary biomarkers for prediction of diabetic kidney disease (DKD). Methods: The cross-sectional study recruited 1053 hospitalized patients with type 2 diabetes mellitus (T2DM), who were categorized into the diabetes mellitus (DM) with normoalbuminuria (NA) group ( n = 753) and DKD group ( n = 300) according to 24-h urinary albumin excretion rate (24-h UAE). Data on the levels of six studied urinary biomarkers [transferrin (TF), immunoglobulin G (IgG), retinol-binding protein (RBP), β-galactosidase (GAL), N-acetyl-beta-glucosaminidase (NAG), and β2-microglobulin (β2MG)] were obtained. The propensity score matching (PSM) method was applied to eliminate the influences of confounding variables. Results: Patients with DKD had higher levels of all six urinary biomarkers. All indicators demonstrated significantly increased risk of DKD, except for GAL and β2MG. Single RBP yielded the greatest area under the curve (AUC) value of 0.920 compared with the other five markers, followed by TF (0.867) and IgG (0.867). However, GAL, NAG, and β2MG were shown to have a weak prognostic ability. The diagnostic values of the different combinations were not superior to the single RBP. Conclusions: RBP, TF, and IgG could be used as reliable or good predictors of DKD. The combined use of these biomarkers did not improve DKD detection.

Aims/IntroductionHyperuricemia (HUA) occurs because of decreased excretion of uric acid, increased synthesis of uric acid or a combination of both mechanisms. The proportions of these three types of HUA in type 2 diabetes patients are not known. In the mean time, we assume that different types of HUA might manifest with different renal damage, even in patients with normal renal filtration function.Materials and MethodsWe included 435 inpatients with type 2 diabetes at the Metabolic Disease Hospital of Tianjin Medical University from 2015 to 2016. Based on the clearance of uric acid, 90 patients with HUA were divided into three types: synthesis‐increased HUA, excretion‐decreased HUA and mixed type of HUA.ResultsPatients with the mixed type of HUA had the severest kidney injury manifested by a high level of 24 h urinary microalbumin, urinary immunoglobulin G, transferrin, α‐galactosidase and β2‐microglobulin compared with the normal uric acid group. Urinary immunoglobulin G, transferrin and α‐galactosidase were also increased in patients with synthesis‐increased HUA compared with the normal uric acid group. Patients with excretion‐decreased HUA did not have an increased level of renal impairment markers; however, these patients had an increased body mass index, which might cause dysfunction of kidney excretion.ConclusionsExcretion‐decreased HUA is a more common type of HUA in type 2 diabetes patients that might be caused by dysfunction of tubular excretion instead of structural damage. The mixed type of HUA patients had the severest kidney glomerular and tubular damage compared with the normal uric acid group. Clinically, different types of hyperuricemia should be given individualized treatment according to their own characteristics.

Background: Increasing evidence indicates that impaired glucose tolerance (IGT) is independently associated with chronic kidney disease, but the characteristics and underlying mechanisms remain largely unknown. Methods: Here, the cross-sectional study was performed to study the characteristics of IGT-induced renal injury (IGT-RI). Furthermore, urine microRNA profile was evaluated and microRNAs involved in tubular injury were determined by in-vitro experiments. Results: It was found that 12.1% of IGT patients had microalbuminuria, which we termed “IGT-RI.” Overall, 100% of patients with IGT-RI exhibited reabsorption dysfunction and 58.3% had structural damage in the renal tubules. Two-hour postprandial insulin, retinol-binding protein, and N-acetyl-β-glucosaminidase were significantly associated with microalbuminuria and they were independent risk factors for IGT-RI. The expression of mir-7977 was altered in IGT-RI patients and may be involved in cellular response to oxidative stress. In proximal tubule epithelial cells in vitro, a high level of insulin increased the expression of mir-7977 and decreased that of sirtuin 3 (SIRT3), leading to oxidative stress. Overexpression of mir-7977 further decreased SIRT3 expression, whereas inhibition of mir-7977 had the opposite effect. Furthermore, mir-7977 can bind to the 3′-untranslated region of SIRT3 mRNA and inhibit its expression. Moreover, inhibition of SIRT3 reduced the expression of cubilin and the endocytosis of albumin. Conclusions: In conclusion, IGT-RI mainly manifests as tubular injury, especially reabsorption dysfunction. Compensatory hyperinsulinemia may be involved. A high level of insulin can activate mir-7977/SIRT3 signaling, resulting in tubular injury by inducing oxidative stress as well as reabsorption dysfunction by inhibiting the expression of cubilin, ultimately contributing to IGT-RI.