Pathologic Findings of Membranoproliferative Glomerulonephritis

Membranoproliferative glomerulonephritis (MPGN) describes a pattern of glomerular injury with common histologic features of glomerular capillary wall thickening (membrano-) and hypercellularity in the glomerular tufts (-proliferative). MPGN was historically classified into three morphologic types: type I, with presence of immune deposits in the subendothelial and mesangial areas; type II, with electron-dense deposits within the basement membrane; and type III, with complex GBM formation with subendothelial and subepithelial electron-dense deposits that are bridged by intramembranous deposits. MPGN can be primary (or idiopathic, most commonly in children) or secondary to infectious and autoimmune disease. A unifying characteristic of all types of MPGN is hypocomplementemia (low C3). MPGN type II, known as dense deposit disease (DDD), is now considered a separate entity from MPGN types I and III, since it has unique pathogenic and clinical features. The disease is characterized by functional impairment of the glomerular basement membrane (GBM), causing progressive loss of renal function that eventually results in end-stage renal disease (ESRD). Clinical features at first manifestation are hematuria, proteinuria (nephrotic range), impaired renal function and hypertension