Jiao Y, Jiang S, Wang Y, et al. - Findings demonstrate involvement of complement activation in the development of diabetic nephropathy (DN), and disease progression could be accelerated due to activation of the classical complement pathway in glomeruli.

• Researchers investigated the role of the complement system in glomeruli from DN patients using integrated transcriptomic bioinformatics analysis and renal histopathology.

• A total of 47 up- and 48 downregulated genes linked with DN were discovered, and complement-related hub genes included C3, C1QB, and C1QA.

• In Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses, complement activation and humoral immune response were found as the significant oncology terms, with C1QB and C3 positioned at the center of the pathway.

• Concerning renal histopathology, the patients had more severe glomerular classes.

• As shown by multivariate Cox proportional hazards regression, deposition of glomerular C1q and C3 was an independent risk factor for renal failure.

• More chance of progression to kidney failure was noted in patients with high C1q, C3, or C4d expression in glomeruli, whereas glomerular mannose-binding lectin was rare.