Abstract

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease. A great number of metabolites, cytokines, proteins and transcription factors play a role in the accumulation of extracellular matrix and mesangial proliferation in the glomerulus. The integrative analysis of the proteomic and transcriptomic features of bioptic samples among different categories of patients affected by diabetic nephropathy, especially based on the accurate classification of the histopathological changes in the glomerular and tubulointerstitial compartment, could lead to the identification of new early biomarkers. Microarray data obtained from glomeruli isolated from normal kidneys (n = 2) and kidneys from patients with DKD (n = 4) were used for the Clariom™ D Assay. The DKD group was further divided into two parts: heavy(type IV stage DN,proteinuria>4g/24 h;n=2 );light (type IIb stage DN,proteinuria<4g/24 h;n=2 ). In the present study, differentially expressed genes (DEGs) between healthy controls and patients with different stages of DN were also analyzed. Two patients were diagnosed as type IIb stage DN with moderate proteinuria, while other two patients were diagnosed as type IV stage DN with massive proteinuria. In the present study, differentially expressed genes (DEGs) between healthy controls and patients with different stages of DN were also analyzed. To investigate the function changes in the course of DN progression, GO enrichment and KEGG pathway analyses were performed for both up- and down-regulated DEGs. GO provides 3 structured networks of de ned terms to describe gene product attributes: cellular compartment (CC), biological process (BP) and molecular function (MF). Results show that signaling pathways are altered by the up-regulated DEGs light_vs_NCView Large Image Figure ViewerDownload Hi-res image Download (PPT)View Large Image Figure ViewerDownload Hi-res image Download (PPT) In conclusion, our transcriptome based analysis suggests that the association between gene expression and renal pathology is mediated by structural changes and that there may be differences in pathways that lead to protenuria.

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