ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: FR-PO836

RNA Sequencing Identifies Novel Genes Implicated in the Pathogenesis of IgA Nephropathy

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Xu, Ricong, The First Affiliated Hospital of Shenzhen University, The Shenzhen Second People's Hospital, Shenzhen, China

IgA nephropathy (IgAN) is one of the most common form of glomerulonephritis throughout the world and also the leading cause of kidney failure among Asian populations. Previous genetic studies have identified several genetic factors predisposing to IgAN, however, the transcriptome changes of kidney tissue of IgAN are not thoroughly investigated yet, which was crucial for the exploration of the molecular pathogenesis of this disease.


We used RNA-sequencing to study the whole transcriptome of kidney biopsies of 8 IgAN patients and 5 control samples. Differentially expressed genes (DEG) were identified using DESeq2. GO and pathway enrichment analysis were applied to explore the biology relevance of these DEGs to IgAN.


We identified 54 genes with differential expression between the IgAN patients and the healthy controls, with 41 genes were up-regulation and 13 were down-regulation in the IgAN patients (fold change >1.5 and FDR<0.1). Pathway enrichment analysis revealed that these DEGs were involved in cotranslational protein targeting to membrane, humoral and innate immune response and endothelium development. Among these, the top of six susceptible genes (P<1×105) were MMP7, SERPINA3, SLPI , RPS27A, FLT1 and NES, which were related to renal fibrosis, innate mucosal defense, angiotensin II production, and endothelial cell proliferation, indicating that they might participate in the pathogenesis of IgAN.


We found 54 genes were dysregulated in the kidney biopsies of IgAN patients, which provided new insights into the molecular pathogenesis of IgAN.