title: The primary glomerulonephritides: a systems biology approach.
abstract: Our understanding of the pathogenesis of most primary glomerular diseases, including IgA nephropathy, membranous nephropathy and focal segmental glomerulosclerosis, is limited. Advances in molecular technology now permit genome-wide, high-throughput characterization of genes and gene products from biological samples. Comprehensive examinations of the genome, transcriptome, proteome and metabolome (collectively known as omics analyses), have been applied to the study of IgA nephropathy, membranous nephropathy and focal segmental glomerulosclerosis in both animal models and human patients. However, most omics studies of primary glomerular diseases, with the exception of large genomic studies, have been limited by inadequate sample sizes and the lack of kidney-specific data sets derived from kidney biopsy samples. Collaborative efforts to develop a standardized approach for prospective recruitment of patients, scheduled monitoring of clinical outcomes, and protocols for sampling of kidney tissues will be instrumental in uncovering the mechanisms that drive these diseases. Integration of molecular data sets with the results of clinical and histopathological studies will ultimately enable these diseases to be characterized in a comprehensive and systematic manner, and is expected to improve the diagnosis and treatment of these diseases.
authors.affiliation: Research Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine, 305 East Zhongshan Road, China.
authors.forename: Song
authors.initials: S
authors.lastname: Jiang
authors.forename: Peter Y
authors.initials: PY
authors.lastname: Chuang
authors.forename: Zhi-Hong
authors.initials: ZH
authors.lastname: Liu
authors.forename: John C
authors.initials: JC
authors.lastname: He
mesh_terms: D000818:Animals; D020869:Gene Expression Profiling; D055106:Genome-Wide Association Study / Q000379:methods*; D005921:Glomerulonephritis / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000473:pathology*; D008954:Models, Biological; D049490:Systems Biology / Q000379:methods*