This study examined the role of local complement synthesis in a mouse model of glomerulonephritis, which evolves into progressive tubulointerstitial disease. The model was used to quantitate clinical, histologic, and transcriptomic outcomes, and assess the role of angiotensin conversting enzyme (ACE) inhibition in modifying these measures. We also comprehensively explored the biological pathways and networks exhibiting alterations in gene expression to provide further insight into the role of ACE inhibition in the model. Overall design: C57BL/6 mice were purchased from The Jackson Laboratories (Bar Harbor, ME). Glomerulonephritis (GN) was induced by the intraperitoneal (IP) injection of 10 mg horse spleen apoferritin (HSA; Sigma, St. Louis, MO) five times weekly for six weeks. Lipopolysaccharide (LPS from Salmonella Minnesota; EMD Biosciences, La Jolla, CA) at a dose of 100 micrograms was also given IP three times weekly as adjuvant, also for six weeks. Control mice received equivalent volumes of normal saline IP on the same schedule. At 9 weeks, mice were euthanized by CO2 inhalation and small sections of kidney cortex (20-30 mg) processed for RNA-sequencing.