A group from Ohio State University Wexner Medical Center, etc. has reported that excess compliments are deposited in Membranous Nephropathy (MN).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7879111/pdf/main.pdf
Glomeruli tissue samples were captured by laser microdissection, and IgGs and complements in the samples were analyzed by mass spectrometry comprehensively. As a result, elevated glomerular levels of all complements (except for CR1) and IgG1~IgG4 were observed in MN patients comparing with health controls. On the other hand, mannose-binding lectin (MBL), Ficolin, and Collectin were not detected. These results suggest that Glomeruli tissue could be damaged by excessively activated complements not through the lectin pathway. Loss of CR1 at the site of the damaged filtration barrier might accelerate excess complement activation resulting in significant damages. In addition, it is thought that M-type phospholipase A2 receptor (PLA2R) could be an antigen in membranous nephropathy.
