question about UW 3946

[250256]

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In this case , the 40 ys old man show nephrotic syndrome. EM of biopy shows dense deposits within glomerular basement membrane. Immunoflurescense show posivtive C3 without Ig. This patient shows no risk fact such as hepatitis HIV or tumor. the answer is membranoproliferative glomerulonephritis.

In the explanation, they mention that membranoproliferative glomerulonephritis is caused by IgG antibody against C3 convertase.

My question is that since this disease is caused by IgG antibody against convertase, why there is no Ig under flurescence microscope? Is this because the Ig does the work in serum but not directly deposit in basement? I can not find the answer in textbook. Waiting for help!

Thanks!

 

[Transposony]

Absence of circulating immune complexes is a unique feature of MPGN type II (or dense deposit disease) which differentiate it from MPGN type I & III.

MPGN type II, or dense deposit disease, is a separate entity that has been conventionally classified with MPGN because of the similarities of light microscopic appearance. The pathogenesis of MPGN type II is not known.

This disease is systemic, as evidenced by dense deposits in the kidney, splenic sinusoids, Bruch membrane of the retina, as well as its association with acquired partial lipodystrophy.[4, 5] MPGN type II also has a high incidence of recurrence in renal allografts. The chemical composition and origin of the dense deposits are not known, although bright staining with thioflavine-T and wheat germ agglutinin suggests the presence of N-acetyl-glucosamine. No circulating immune complexes are observed in MPGN type II.

 

[250256]

Absence of circulating immune complexes is a unique feature of MPGN type II (or dense deposit disease) which differentiate it from MPGN type I & III.

Thank you, Transposony!