The presence of C3 without significant immunoglobulin suggested to early investigators that DDD was due to abnormal activation of the complement alternative pathway (AP).

[11] In many cases, people with MPGN II can develop drusen caused by deposits within Bruch's membrane beneath the retinal pigment epithelium of the eye.

Over time, vision can deteriorate, and subretinal neovascular membranes, macular detachment, and central serous retinopathy can develop.

[12] Type III is very rare, it is characterized by a mixture of subepithelial and subendothelial immune and/or complement deposits.

[citation needed] It also is related to a number of autoimmune diseases, prominently systemic lupus erythematosus (SLE), Class IV.

[citation needed] The GBM is rebuilt on top of the deposits, causing a "tram tracking" appearance under the microscope.