Focal segmental glomerulosclerosis induces gut microbiome dysbiosis in mice

Background Focal Segmental Glomerulosclerosis (FSGS) is a chronic kidney disease characterized by progressive scarring of the glomeruli. It is classified into primary and secondary forms, with secondary FSGS arising from various factors including genetic predisposition. This study aimed to investigate gut microbiota's role in FSGS, particularly in an Adriamycin-induced mouse model, to understand its potential impact on the disease's pathophysiology.p Methods Four male BALB/c mice were used per group. FSGS was induced in the treatment group via Adriamycin administration, with the control group receiving saline. Stool samples were subsequently collected, and genomic DNA was extracted. Following stringent quality control measures to ascertain DNA integrity, comprehensive metagenomic shotgun sequencing was conducted to support downstream analyses. Results Co-abundance group (CAG) analysis revealed a significant increase in specific taxonomic classification CAG 168. Although no significant differences in α-diversity at any taxonomic level, β-diversity analysis showed marked alterations in microbiota composition at genus and species levels in diseased mice. Notably, the taxonomic classifications at the species level showed a statistically significant elevation in the relative abundance of Alistipes_MGG05257, UBA3263_sp001689615, and UBA3282_MGG00857 in the disease-induced group, suggesting a potential link to the disease. Discussion and Conclusion The study highlights a significant shift in gut microbiota composition associated with FSGS. These findings suggest a potential defensive mechanism against kidney injury and underscore the importance of understanding gut microbiota dynamics in FSGS. The study opens new avenues for exploring the functional roles of identified taxa in FSGS pathophysiology.