Abstract: TH-PO034

Fecal Microbiome Profiles and Pathogenesis of IgA Nephropathy

Session Information

Category: Glomerular

  • 1001 Glomerular: Basic/Experimental Immunology and Inflammation

Authors

  • Park, Ji In, Kangwon National University Hospital, Chuncheon-si,, Korea (the Republic of)
  • Cho, Hyunjeong, Seoul National University Hospital, Seoul, Korea (the Republic of)
  • Lee, Hajeong, Seoul National University College of Medicine, Seoul, Korea (the Republic of)
  • Kim, Dong Ki, Seoul National University Hospital, Seoul, Korea (the Republic of)
  • Yang, Seung Hee, Kidney Research Institute, Seoul National University, Seoul, Korea (the Republic of)
  • Lee, Jung Pyo, Seoul National University Boramae Medical Center, Seoul, Korea (the Republic of)
  • Kim, Yon Su, Seoul National University College of Medicine, Seoul, Korea (the Republic of)
Background

Mucosal immune system plays a role in pathogenesis of Immunoglobulin A nephropathy (IgAN); however, little has been known about the relationship between IgAN and the intestinal microbiome.

Methods

We prospectively enrolled 30 biopsy-proven IgAN patients at 3 centers and collected fecal specimens at the time of renal biopsy. Feces from thirty healthy volunteers were used as control. The composition of microbiota was analyzed using extracted metagenomic DNA from the feces by Illumina MiSeq system. Downstream analyses were performed using SPSS, Phylogenetic reconstruction of unobserved states (PICRUSt), and Linear discriminant analysis Effect Size (LEfSe).

Results

The age, sex, and BMI were comparable between the groups. The fecal microbiota of both IgAN and control group were dominated by two bacterial phyla, Firmicutes and Bacteroidetes. Compared to control group, fecal microbiota of IgAN patients showed significantly lower OTUs and Shannon diversity index. The relative abundances of Firmicutes and Acinetobacteria were higher, whereas those of Bacteroidetes and Proteobacteria were lower in IgAN patients than healthy subjects. At Genus level, the abundances of Blautia were higher and those of Bacteriodetes, Prevotella, and Escherichia were lower in the fecal specimens from IgA nephropathy patients compared to healthy subjects.
PICRUSt analysis showed that genes involved in galactose metabolism were enriched in IgAN while those responsible for glycosyltransferases were significantly associated with the controls.
By dividing patients on the basis of 3 g/day proteinuria, bacterial diversity was significantly lower in severe group compared to less severe group.

Conclusion

The fecal microbiota of IgAN patients differed from those of control group. We also showed that microbial difference was possibly related to galactose metabolism or glycosyltransferases. Such differences might be related with pathogenesis of IgAN.