Identification of key genes and pathways in IgA nephropathy using bioinformatics analysis

IgA nephropathy (IgAN) is the most frequent type of primary glomerulonephritis globally and the leading cause of end-stage renal disease in young adults. Its pathogenesis is not fully known, but is largely attributed to genetic factors. This study was aimed to explore the prognostic values of key genes in IgAN.

The gene expression profile GSE93798 of 20 IgAN samples and 22 normal samples using glomeruli from kidney biopsy was adopted. Totally 447 upregulated and 719 downregulated differentially expressed genes were found in IgAN patients on the R software. The Gene Ontology enrichment and the Kyoto Encyclopedia of Gene and Genomes pathway were investigated on DAVID, and the protein-protein interaction network and the top 13 hub genes of the differentially expressed genes were built via the plug-in molecular complex detection and cytoHubba of Cytoscape.

From the protein-protein interaction network, of the top 13 hub genes, FOS, EGFR, SIRT1, ALB, TFRC, JUN, IGF1, HIF1A, and SOCS3 were upregulated, while CTTN, ACTR2, CREB1, and CTNNB1 were downregulated. The upregulated genes took part in the HIF-1 signaling pathway, Choline metabolism in cancer, Pathways in cancer, Amphetamine addiction, Estrogen, TNF, and FoxO signaling pathways, and Osteoclast differentiation, while the downregulated genes were involved in Pathogenic Escherichia coli infection, Bacterial invasion of epithelial cells, prostate cancer, and melanogenesis.

This study based on the Gene Expression Omnibus database updates the knowledge about the mechanism of IgAN and may offer new treatment targets.