Glomerular Diseases Please Someone help!

[StressedMedStud]

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I am having trouble understanding what the differences are between:

1. Diffuse Proliferative Glomerulonephritis
2. Membranous Glomerulonephritis aka Diffuse Membranous Glomerulonephropathy
why is this associated with spike and dome? what is actually spiked and domed?

3. Membrano-proliferative Glomerulonephropathy Type 1 and Type 2.

Can anyone please break this down for me? I read FA and Kaplan physio book but they dont explain well for examply why you see spikes and domes in membranous, I want to understand this infomration not just memerozie key facts about each disease.

The only things I know are that diffuse means it affects all the glomerulus, membranous means it affects basement membrane and that becomes thick,

I DONT understand proliferative though. In FA it says it means hypercellular glomeruli but I dont understant that? Does this have to do with mesangium?

Last questions I dont really get Mesangium? Is it the support structure of capillaries?

 

[tjquinn]

I am having trouble understanding what the differences are between:

1. Diffuse Proliferative Glomerulonephritis
2. Membranous Glomerulonephritis aka Diffuse Membranous Glomerulonephropathy
why is this associated with spike and dome? what is actually spiked and domed?

3. Membrano-proliferative Glomerulonephropathy Type 1 and Type 2.

Can anyone please break this down for me? I read FA and Kaplan physio book but they dont explain well for examply why you see spikes and domes in membranous, I want to understand this infomration not just memerozie key facts about each disease.

The only things I know are that diffuse means it affects all the glomerulus, membranous means it affects basement membrane and that becomes thick,

I DONT understand proliferative though. In FA it says it means hypercellular glomeruli but I dont understant that? Does this have to do with mesangium?

Last questions I dont really get Mesangium? Is it the support structure of capillaries?

1. Diffuse proliferative glomerulonephritis is the diffuse deposition of antigen-antibody complexes associated with sub-endothelial deposits seen in SLE.

2. Membranous Nephropathy - It is not absolutely clear what "causes" this, but the association is with Hepatitis B (and C), solid tumors, SLE (nephrotic range this time), or drugs. The result is subepithelial deposits of immune complexes. Subepithelial refers to the deposits getting stuck under the podocytes (which comprise the epithelial). As a result, these deposited immune complexes disrupt the the smooth interaction of the podocyte with the basement membrane, so more BM is laid down to fill in the gap between adjacent immune complexes. Consequently, when you silver stain, the BM will turn black and the deposits will not. As the process continues, the laid down BM will overcome the subepithelial deposits and the image will be a spike (corresponding to BM laid down between adjacent immune complexes) and dome (corresponding to BM that has laid down such that it now covers the immune complex):

|OVO|

3. Membranoproliferative Glomerulonephritis - If the immune complexes deposit within the BM, then it is Type II; and if they are deposited subendothelially then it is type I. In both cases the membrane is thickened. The proliferative does in fact refer to the mesangium, which is the structural support of glomerulus. Mesangial cells produce the BM and they have contractile function to manage how the glomerulus functions. T

 

[StressedMedStud]

1. Diffuse proliferative glomerulonephritis is the diffuse deposition of antigen-antibody complexes associated with sub-endothelial deposits seen in SLE.

2. Membranous Nephropathy - It is not absolutely clear what "causes" this, but the association is with Hepatitis B (and C), solid tumors, SLE (nephrotic range this time), or drugs. The result is subepithelial deposits of immune complexes. Subepithelial refers to the deposits getting stuck under the podocytes (which comprise the epithelial). As a result, these deposited immune complexes disrupt the the smooth interaction of the podocyte with the basement membrane, so more BM is laid down to fill in the gap between adjacent immune complexes. Consequently, when you silver stain, the BM will turn black and the deposits will not. As the process continues, the laid down BM will overcome the subepithelial deposits and the image will be a spike (corresponding to BM laid down between adjacent immune complexes) and dome (corresponding to BM that has laid down such that it now covers the immune complex):

|OVO|

3. Membranoproliferative Glomerulonephritis - If the immune complexes deposit within the BM, then it is Type II; and if they are deposited subendothelially then it is type I. In both cases the membrane is thickened. The proliferative does in fact refer to the mesangium, which is the structural support of glomerulus. Mesangial cells produce the BM and they have contractile function to manage how the glomerulus functions. T

Thank you for taking the time to respond! These concepts are becomin more clear to me now! 🙂

 

[StudentDoctorM]

Sorry to revive this old post, but I also keep having trouble understand the pathophys of these glomerular diseases.. could someone explain what leads to the subendothelial deposits, as compared to subepithelial deposits? and what is causing the mesangial proliferation..? is it due to any kind of inflammation?

Thanks in advance

 

[aspiringmd1015]

mesangium proliferates in type 1 MPGN in response to the deposition of these immune complex deposits, which then causes the classic tram-track appearance