Abstract
IgA nephropathy represents a significant challenge in nephrology research, and an understanding of its underlying molecular mechanisms is crucial. In this study, we conducted a comprehensive proteomic investigation of IgA nephropathy utilizing microdissection techniques combined with data-independent acquisition technology. Our analysis focused on differentially expressed proteins in the glomeruli, interstitium, and tubules of the kidney. Functional enrichment analysis revealed distinct pathway enrichment patterns, with fatty acid synthesis predominating in the glomerulus and complement and coagulation pathways predominantly enriched in the tubules. These pathway enrichments suggest potential key contributors to the pathogenesis of IgA nephropathy. Furthermore, our study identified ATP1B1 and COX4I1 in the glomerulus and SLC22A13 in the tubules as promising diagnostic markers for the disease. Meanwhile, C4A and APEX1 proteins were identified as valuable biomarkers for assessing disease progression. This research could provide valuable insights into the proteomic alterations associated with IgA nephropathy and offer potential targets for further therapeutic exploration.