Glomerular diseases
Vložit
- čas přidán 23. 07. 2024
- This is a summary of diseases that affect the glomerulus of the kidney, including those that case nephrotic and nephritic syndromes.
I created this presentation with Google Slides.
Image were created or taken from Wikimedia Commons
I created this video with the CZcams Video Editor.
ADDITIONAL TAGS:
Glomerular diseases
Minimal change disease
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
Diabetic nephropathy
Amyloid nephropathy
Lupus nephritis
Membranoproliferative glomerulonephritis
IgA nephropathy
Acute postinfectious glomerulonephritis
Anti-GBM disease
ANCA glomerulonephritis
Nephrotic
Nephritic
Systemic
Primary glomerular disease with nephrotic syndrome
Most common in children, especially young children
LM: “minimal change†-- looks normal
IF: negative (no immune complex deposition)
EM: foot process effacement, see figure
secondary causes: cancer, infection, drugs, atopy (hyperallergic)
Associated with lymphoma and use of NSAIDs
Primary glomerular disease with nephrotic syndrome
Focal means some glomeruli, segmental means not all of glomerulus
LM: segmental glomerular scarring, see hyaline material (deposits from plasma)
IF: positive for Ig and complement, granular appearance
EM: segmental effacement
Primary FSGS is idiopathic
Secondary causes: genetic, infection (HIV, parvovirus), drugs (heroin), sickle cell, obesity
Most common in blacks
Primary glomerular disease with nephrotic syndrome
LM: capillary wall thickening with IgG and C3 immune complexes
IF: positive for IgG and C3 in the capillary, granular
EM: immune complexes in subEPIthelial space
Primary cause: Ab against anti-phospholipase A2 receptor
Secondary causes: cancer, lupus, NSAIDs, HBV, Hep B, syphilis… Ag can be Hep B or cancer
Secondary nephropathy with nephrotic syndrome; DM is primarily systemic disease
Caused by DM types I and II → accumulation of glycosylated plasma protein in GBM and mesangium
LM: mesangial expansion and KW nodules
IF: linear staining of IgG
EM: thickened GBM
Treatment is reduce blood sugar, lower blood pressure, avoid nephrotoxins
Most common cause for end stage renal disease in United States
Secondary nephropathy with nephrotic syndrome; amyloidosis is primarily a systemic disease
Caused by accumulation of polypeptides (especially AL and AA amyloid)
LM: thickening of mesangium amorphous pale pink stuff in glomerulus, confirm with Congo Red stain
IF: monoclonal staining of accumulated amyloid protein
EM: randomly arranged fibrils
Associated with rheumatoid arthritis and multiple myeloma
Ranked by class: I (best) to VI (worst)
Antigen antibody complexes deposit in gloms, activate complement which leads to proliferation of mesangium and infiltration of PMNs
LM: endocapillary and mesangial proliferation and sometimes crescents
IF: granular pattern, everything lights up! “full house patternâ€
EM: deposits anywhere and everywhere
Hypocomplementemia - both C3 and C4 blood levels are low
Presents with nephritic and/or nephrotic syndrome; kind of in between
Type I is immune complex and C3 deposits
Caused by bacterial infection, hep C infection, malignancies
Type II is just C3 deposits but no Ig
Caused by complement dysregulation
LM: capillary wall thickening with hypercellularity
IF: immune complexes and/or C3 granular deposits
causing hypocomplementemia
EM: same deposits (subendo and BM)
Deposits of IgA alone or with other Igs, in mesangium
Activates complement, which causes proliferation of mesangial cells
LM: mesangial hypercellularity
IF: IgA positive, granular pattern in the mesangium
EM: mesangial deposits
Primary IgA nephropathy is idiopathic
Can be part of systemic disease IgA vasculitis; related to Henoch– Schönlein purpura
Occurs few weeks after infection; most often follows strep or staph
LM: endocapillary and mesangial hypercellularity and PMNs
IF: pos for C3 in capillary walls, granular
EM: subepithelial humps
Hypocomplementemia; low C3 levels
Treatment is supportive
Nephritic
Caused by autoAb to glomerular basement membrane
Abs recruit complement and lymphocytes → damages capillary → proliferation and accumulation in Bowman’s space → crescent
LM: crescent formation
IF: pos for IgG in linear pattern
EM: normal
Disease is called Goodpasture’s syndrome when presents with both kidney and lung involvement
LM: crescents, necrosis
IF: pauci-immune; not much lights up
EM: normal
Associated diseases:
Granulomatosis with polyangiitis (GPA); Wegener's; PR3
Eosinophilic granulomatosis with polyangiitis (eGPA); Churg–Strauss churg Strauss
Microscopic polyangiitis (MPA)
You've genuinely saved me with your videos, clear cut, straight to the point. They're time savers, and I learn all the essentials without having to plough through notes for hours. You deserve way more subs, thank you so much!
This is beyond helpful, clear, and explanatory! Thank u so muchhh
Thank you for your presentation.
You are amazing.
That's a summary and that's what you need all
excellent. thank you.
Very helpful,thank you
Simply Amazing. You have explained it very well. Mind you this is a very tough topic to teach.
Great video man !! :))
Very helpfull ,thanks
Very helpful!
Very infomative video
this video is one of the best clips I have ever seen👍
amazing thank u !
Aptly described👌👌👌👌👌👌👌
Brilliant 🤩
thank you so much, very helpfull
,May i please get the slide?
Great!!!!!!
which category does Fibrillary Glomerulonephritis fall into ? thank you
Bravo.
can u please share with us those amazing slides?
My ex agony
Thank you kind soul
thank you for the summary🙏, I think it would be better to label the histopathologies so that the damage is more understood, but other than that thank you sir 👌
Hey, does acute glomerulonephritis always present as nephritic syndrome? Or could it be nephrotic too? Thanks a lot in advance. This doubt has been bugging me for days. I've searched quite a bit and different books state different things. I'd appreciate if you replied. Thanks again! And great work on all your videos.
Does ur Albumin leak? I have same problem too. Any solution ?
I love you
Really useful video thanks a lot!
can you please explain what are you seeing in the slides? where are the foot processes? the biggest problem for me is seeing it on the histology slides
Quite sure that diabetic nephropathy comes up negative on IF
its never lupus fr
great presentation except for the fact that you referred to african americans/people of african descent as blacks which is disrespectful. no one refers to Asians as ''yellows''. no one refers to caucasians as ''whites''.
There's no such thing as "african americans" or "people of african descent", those are made up terms of little relevance, they're black, end of story. Yes, we do refer to whites as whites in medicine. And blacks as blacks. Race has nothing to do with nationality or the continent someone is from.There are black people who AREN'T African or American.
lol the guy made a good video and posted it where everyone can have acess to it. Forget race. I am African American or Blacks whatever.....I migrated from Africa to America and I have no slave blood in me. I think all that is nonsense. Great video please keep teaching me. I want to wash my ignorance away compare to some people. just had to comment. sorry. it just irk me.
slave blood? jokes on you
People call caucasians whites all the time. Stop looking to be offended, there's no context here to be offended from.
Everyone refers to Caucasians as whites