There are three types of MPGN, but this classification is becoming obsolete as the causes of this pattern are becoming understood.
Type I Type I, the most common by far, is caused by
immune complexes depositing in the kidney. It is characterised by subendothelial and mesangial immune deposits. It is believed to be associated with the
classical complement pathway.
Type II – Dense deposit disease Type II is today more commonly known as
dense deposit disease (DDD). Most cases of dense deposit disease do not show a membranoproliferative pattern. It forms a continuum with
C3 glomerulonephritis; together they make up the two major subgroups of
C3 glomerulopathy. Most cases are associated with the dysregulation of the
alternative complement pathway. DDD is associated with deposition of complement C3 within the glomeruli with little or no staining for immunoglobulin. The presence of C3 without significant immunoglobulin suggested to early investigators that DDD was due to abnormal activation of the complement alternative pathway (AP). There is now strong evidence that DDD is caused by uncontrolled AP activation. Spontaneous remissions of MPGN II are rare; approximately half of those affected with MPGN II will progress to
end stage renal disease within ten years. 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.
Type III Type III is very rare, it is characterized by a mixture of subepithelial and subendothelial immune and/or complement deposits. These deposits elicit an immune response, causing damage to cells and structures within their vicinity. Has similar pathological findings of Type I disease. A candidate gene has been identified on
chromosome 1.
Complement component 3 is seen under
immunofluorescence. it is associated with complement receptor 6 deficiency. ==Pathology==