multiple injured glomeri show extensive involvement by cellular crescents, in a background of tubulointerstitial injury; crescents on early biopsy are a feature suggestive of a poor prognosis

Cellular crescent envelops a hypercellular glomerulus with closed capillary loops

Marked endocarpillary hypercellularlity composed of endocapillary proliferation and inflammatory cells. Thickened capillary walls are appreciated on this higher magnification

C3 shows a bright ribbon-like pattern outlining the glomerular basement membranes.

another case Image

thickened basement membrane Image

PAS nice Image

MPGN II can be associated with acquired partial lipodystrophy (APL)

M=F. Very rare.

Commonly affects children and young adults

Present with proteinuria and/or hematuria to varying degrees

often have hypocomplementemia

can screen for 'C3 nephritic factor' - an autoantibodies directed against C3bBb, the convertase of the alternative pathway (AP) of the complement cascade.

Distinguishing DDD from membranoproliferative glomerulonephritis type I may not be possible clinically since both are characterized by a nephrotic and/or nephritic clinical picture. In actuality, there aremarked differences in etiology and pathogenesis between type I membranoproliferative glomerulonephritis and dense deposit disease.

Spontaneous remission almost never occurs. The more likely outcome is chronic deterioration of renal function leading to renal failure in approximately half of patients within 10 yr (Appel). In others, rapid fluctuations in proteinuria occur with episodes of acute renal deterioration in the absence of obvious triggering events; others may manifest a more stable pattern for years despite persistent proteinuria (Appel).