Prior studies showed that the intrinsic kidney tubular epithelial cells and interstitial kidney cells express high level of complement genes such as C1q, C1r, C1s and C3 (5), which could cause kidney damage through the following potential mechanisms: 1) cytokine production contributing to interstitial inflammation (12), 2) direct stimulation of extracellular matrix production (12–15) and 3) activation of the renal renin angiotensin system (16). This evidence concerns the gene C3 and Nephropathy.