Membranous nephropathy and membranoproliferative glomerulonephritis

[chromuffin]

Both can be caused by HBV or HCV. Membranous nephropathy causes subepithelial deposits. Membranoproliferative GN Type I causes subendothelial deposits. Would it be incorrect to assume that a HCV infected patient presenting with 3+ proteinuria could have membranous nephropathy AND membranous GN Type I? Or is this a "one or the other" condition? This is all hypothetical, I haven't received any question stems about this.

Also..
Having some difficulty in knowing what exactly causes the tram track appearance on membranoproliferative GN and what exactly Type II is.. "dense deposit" doesn't really indicate location. Is it just all over (i.e. Subepi and sub Endo)? Is it within the Type 4 collagen (as suggested by "intramembranous" in pathoma)?

Thanks!

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[Beezlebub]

1) Tram track appearance in MPGN I is mesangial cells (basically macrophage-like function) invading the GBM, creating a double contour appearance on EM
2) Dense deposit spans the entire GBM and tubular membrane (therefore "intramembranous"), indicative of MPGN II. Deposits in subepi is usually post strep; subendo is generally lupus. hope that clears it up.

 

[Transposony]

what exactly causes the tram track appearance on membranoproliferative GN

 

[Beezlebub]

what exactly causes the tram track appearance on membranoproliferative GN

thanks for the clarification. Always thought of those mesangial cells as macrophages.

 

[chromuffin]

what exactly causes the tram track appearance on membranoproliferative GN

So then the mesangial cells destroy the GBM, causing there to be BM remodeling over the immune complexes and where the initial BM was located?

 

[Transposony]

So then the mesangial cells destroy the GBM, causing there to be BM remodeling over the immune complexes and where the initial BM was located?

Splitting of BM is caused by interposition of mesangial cell processes and/or due to new basement membrane synthesis in response to subendothelial deposits of immune complexes.
In other words, mesangial cell is trying to get rid of the "deposits" using it's "arms & hands" and end up splitting BM same way you "split" your skin while trying to get rid of a splinter lodged in the skin layer.