Complement 3 glomerulopathy (C3G) is a rare, complement-mediated kidney disease characterized by overactivation of the alternative pathway (AP). C3G encompasses 2 subtypes—dense deposit disease and C3 glomerulonephritis—both of which lead to C3 deposition in the glomeruli, progressive kidney dysfunction, and, ultimately, kidney failure. The pathophysiology of C3G and the underlying complement AP overactivation are often driven by genetic mutations and/or acquired autoantibodies. These systemic drivers can affect both native and transplanted kidneys; thus, C3G is associated with a high risk of recurrence in allografts.