Abstract

ObjectiveDiabetic nephropathy (DN) is a leading cause of end-stage renal disease. Since there are limited therapeutic options available for the prevention of DN progression, it is imperative to explore novel differentially expressed genes and therapeutic targets for DN. MethodsIn this study, mice kidney tissue were subjected to transcriptome sequencing and the results were analysed using bioinformatics methods. Interleukin 17 receptor E (IL-17RE) was screened from the sequencing data and its expression was validated in the animal tissues and a cross-sectional clinical study. Fifty-five DN patients were enrolled and further subdivided into two groups based on the urinary albumin-to-creatinine ratio (UACR). Two control groups were used for comparison (minimal change disease group, 12 patients; normal control group, 6 patients). Correlation analysis was conducted to study the relationship between IL-17RE expression and the clinicopathological indices. Logistic regression and receiver operating characteristic (ROC) curve analyses were conducted to evaluate the diagnostic value. ResultsIL-17RE expression was significantly higher in db/db mice and the kidney tissues of DN patients than the control group. IL-17RE protein levels in the kidney tissues were strongly correlated with neutrophil gelatinase-associated lipocalin (NGAL) levels, UACR, and certain clinicopathological indices. IL-17RE levels, total cholesterol (TC) levels, and glomerular lesions were independent risk factors for macroalbuminuria. ROC curves showed a good detection value for IL-17RE in macroalbuminuria (area under the curve = 0.861). ConclusionThe results of this study provide novel insights into DN pathogenesis. Kidney IL-17RE expression levels were associated with DN disease severity and albuminuria.

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