Aims: The negative effect of obesity on kidney health has been reported. The association between weight-adjusted-waist index (WWI, a newly developed adiposity index) and albuminuria has not been reported earlier.Methods: This cross-sectional study was conducted among adults with complete data about WWI and urinary albumin-to-creatinine ratio (ACR) in 2005–2018 National Health and Nutrition Examination Survey (NHANES). WWI was calculated as waist circumference (WC) divided by the square root of weight. Weighted multivariable logistic regression and generalized additive model were employed to explore the independent relationship between WWI with albuminuria and its non-linearity. A two-piecewise linear regression model was used to calculate the threshold effect. Subgroup analysis and interaction tests were also performed.Results: A total of 36,921 participants were enrolled with a prevalence of albuminuria of 9.32%. The prevalence of albuminuria increased with the higher WWI tertiles (Tertile 1: 5.31%, Tertile 2: 8.23%, Tertile 3: 15.65%). WWI was positively associated with a higher likelihood of albuminuria (OR = 1.28, 95% CI: 1.15–1.43), and this relationship remains stable in subgroups (all P for trend > 0.05). Non-linear positive relationships were detected in females with a breakpoint of 10.93. A positive association between WWI and albuminuria (OR = 1.39, 95% CI: 1.20–1.61) was observed on the right of the breakpoint, while the association on the left was of no statistical significance. WWI showed a stronger correlation with albuminuria (OR = 1.28) than other markers of obesity including body mass index (BMI, OR = 1.02) and WC (OR = 1.01).Conclusion: Weight-adjusted-waist index levels were positively related to an increased likelihood of albuminuria in United States adults and showed a stronger relationship than BMI and WC. Our findings indicated that WWI may serve as a simple anthropometric index to predict albuminuria.

MicroRNAs have been demonstrated to play an important role in the pathogenesis of diabetic nephropathy (DN). In this study, we investigated both the repertoire of miRNAs in the kidneys of patients with DN and their potential regulatory role in inflammation-mediated glomerular endothelial injury. The miRNA expression profiling of the renal biopsy samples was performed by a microarray analysis; then, in situ hybridization and real-time polymerase chain reaction (PCR) were used to determine the localization and expression of two of the miRNAs significantly up-regulated in human DN kidney samples, miR-155 and miR-146a, in the kidney tissues from type 1 and type 2 DN rat models. Human renal glomerular endothelial cells (HRGECs) cultured under high-glucose conditions were transfected with miR-155 and miR-146a mimics, and the transforming growth factor (TGF)-β1, tumor necrosis factor (TNF)-α, and nuclear factor (NF)-κB expressions were examined by western blot, real-time PCR, and an electrophoresis mobility shift assay. The expression of both miR-155 and miR-146a was increased more than fivefold in the kidney samples of the DN patients compared with the controls, and the miR-155 expression was closely correlated with the serum creatinine levels (R = 0.95, P = 0.004). During the induction and progression of the disease in type 1 and type 2 DN rat models, miR-155 and miR-146a were demonstrated to increase gradually. In vitro, high glucose induced the over-expression of miR-155 and miR-146a in the HRGECs, which, in turn, increased the TNF-α, TGF-β1, and NF-κB expression. Taken together, these findings indicate that the increased expression of miR-155 and miR-146a in the DN patients and in the experimental DN animal models was found to contribute to inflammation-mediated glomerular endothelial injury.