Background: Focal segmental glomerulosclerosis (FSGS) is a clinicopathological syndrome manifesting glucocorticoid-resistant nephrosis, which requires new therapies targeting specific pathways. The Columbia classification stratifies FSGS into 5 variants: Collapsing, Tip, Cellular, Perihilar and NOS. Differences in their renal prognosis imply distinct underlying molecular mechanisms, which remain unclear.
Objective: To investigate factors associated with the pathogenesis of FSGS and explore potential therapeutic targets.
Methods: A total of 73 kidney biopsy tissues were analyzed by LC-MS/MS: FSGS (n=23), renal donors (n=14) as a healthy control group, and minimal change disease (n=15) and IgA nephropathy (n=21) as disease control groups. We validated the proteome data with immunohistochemistry and the Nephroseq microarray data.
Results: Our proteomics platform identified a total of 4,168 proteins. A comparison between the FSGS with renal donor groups revealed 175 proteins increased
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