Objective: Metabolic syndrome is associated with development of nephropathy. Emerging evidence supports that white adipose tissue (WAT) depots surrounding the organs, such as peri-renal or peri-cardial WAT, are implicated in regulation of the organ function. It has been previously reported that peri-renal fat thickness is an independent predictor of chronic kidney disease in type 2 diabetic patients. However, it is unclear how peri-renal WAT is involved in regulation of renal function. In this study, we utilized a public microarray dataset to identify novel genes and networks regulated by inflammation in peri-renal WAT. Methods: Dataset was obtained from Gene Expression Omnibus (GEO) database. Briefly, adipose tissue-derived mesenchymal stem cells (ASC) isolated from peri-renal WAT were treated with either alloactivated peripheral blood mononuclear cells (PBMC) or with proinflammatory cytokine cocktail (IFNγ, TNFα, IL6) and analyzed by Affymetrix Human Gene array. The dataset was further analyzed to identify differentially expressed genes (DEGs), gene ontology, and gene networks regulated by inflammation. The identified genes were confirmed in peri-renal WAT of patients undergoing renal transplant. Results: In ASCs derived from peri-renal WAT, 707 genes were upregulated and 293 genes were downregulated by cytokine treatment, and 163 genes were upregulated and 127 genes were downregulated by PBMC treatment. Gene set enrichment analysis showed that immune response was upregulated and extracellular matrix organization was downregulated by cytokine treatment whereas chemokine-mediated signaling was upregulated and cell adhesion was downregulated by PBMC treatment. Of note, network analysis revealed that thioredoxin interacting protein (TXNIP)-NLR family, pyrin domain containing 3 (NLRP3) pathway is regulated by inflammation in peri-renal ASCs. Conclusion: Utilization of GEO dataset has revealed novel networks associated with inflammation in peri-renal WAT which may further provide evidence in pathophysiology of renal dysfunction.