Intrarenal complement activation leads to chronic tubulointerstitial injury in animal models of
proteinuric nephropathies, making this process a potential target for therapy. This study
investigated whether a C3-mediated pathway promotes renal injury in the protein overload
model and whether the abnormal exposure of proximal tubular cells to filtered complement
could trigger the resulting inflammatory response. Mice with C3 deficiency were protected to
a significant degree against the protein overload–induced interstitial inflammatory response …