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Glomerular Disease Flashcards

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0
Q

visceral epithelium

A

podocytes; also negatively charged. interdigited with foot process

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1
Q

endothelium

A

fenestrated cytoplasm coated with negatively charged glycoprotein

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2
Q

basement membrane

A

proteoglycans
laminin
collagen IV

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3
Q

what is BM shaped like

A

triple helical alpha molcule

hook like non-collagenous domain

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4
Q

mutations in basement membrane lead to

A

alport syndrome

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5
Q

fx of mesangium

A

cntracts to regulate glomerular blood flow
tethers to GBM to counteract capillary distentsion pressure
produces GFs and cytokines
phagocytoses debris

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6
Q

two types of glomerular injury due to antibodies

A

insitu complex deposition

circuling immune complex nephritis

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7
Q

two types of insitu deposition (ab specific to glom)

A

anti-gbm nephritis

membranous BN

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8
Q

Anti GBM nephritis

A

Ig against NC1 domain of Collagen IV

IF shows LINEAR immune staining

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9
Q

Goodpasture syndrome is a type of ____ that causes_____

A

antiGBM nephritis

cross reaction with alveolar basement membrane

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10
Q

Membranous GN

A

GP330 homolog, Mtype PLA2R–>binding–>C-activation–>subepithelial deposits

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11
Q

circulating immune complex nephritis means that

A

antigens arent specific to glomeruli but end up on GBM because of its properties and hemodynamic factors
EM will show deposits (exo or endogenous) in subepithelial, mesangial, etc
anionic-subendo
cationic-subepithelial
neutral- mesangium

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12
Q

Three component of any kidney biopsy

A

light microscopy
immunofloresence
electromicroscopy

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13
Q

way to classify LMs

A

kidney- focal (some glomeruli) vs difffuse (all glom)

glomerulus: segmental vs global

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14
Q

IF immunocomplex patterns

A

linear- anti GBM disease, light chain deposition (multiple myeloma)
granular- immune complex
nonsepcific patterns

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15
Q

things to evalute on EM

A

e- dense deposits
podocyte charges
GBM alterations

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16
Q

ddx of glomerular disease

A

nephrotic
nephritic
hematuric
rapidly progressive GN

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17
Q

5 types of nephrotic syndrome

A 
minimal change disease
FSGS
membraneous GN
diabetes
amyloidosis
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18
Q

3 types nephritic syndrome

A

post infectious GN
MPGN
lupus nephritis

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19
Q

3 types of hematuric GD

A

alport syndrome
TBM
IgA nephropathy

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20
Q

clinical features of nephrotic sydnrome

A

proteinuria
hypoalbuminemia
edema (decreased oncotic and increased Na retneiton)
hypercholesterolemia (inc prod, dec catabolism)

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21
Q

minimal change disease is the MC of nephrotic syndrome in

A

children

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22
Q

MCD is often secondary to

A

lymphoma, NSAIDs

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23
Q

what will you see on tests with MCD?

A

EM: effacement of foot processes

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24
tests for FSGS
LM: segmental collapse ins caring in SOME glomeruli EM: effacement foot processes, thick BM IF: - except some IgM/C3 trapping
25
FSGS etiology
can be either idiopathic (suPAR) or secondary (family, adaptive, viruses (parvo, hiv), drugs (heroin, lithium)
26
evolution of membranous glomeruopathy
immune complex deposits accumulate--->GBM reacts by forming spike like projects-->grow to spike and dome-->lead to thickened basement membranes
27
MG is the main cause of nephrotic syndrome in
adults
28
etiology of MGNopathy
primary and secondary (drugs, tumors, lupus, infx)
29
tests and MGpathy
LM: suepithelial immune deposits EM-subepithelial spike like projects of GBM IF: diffuse GRANULAR pattern--Igg, c3
30
LM of diabetes early and late
early: glomerular hypertrophy, widened sclerotic mesangium, thickend GBM advanced progressive GBM thickening with KW spots, microaneurysms, arteriolar hylinization
31
EM for diabetes
thick GBM | mesangial sclerosis
32
IF for diabetes
neg for deposits
33
LM for amyloidosis
mesangial and GBM deposition of b pleated amyloid | congo red!
34
EM amyloidosis
8-12 fibrils
35
IF amyloidosis
negative, but lambda chain positive
36
LM acute post-infectious GN
diffuse endocapi. prolif with LEUKOCYTES | swollen, hypercellular glomerulus
37
EM APIG
hump like deposits
38
IF APIG
granular along GBM (c3!)
39
what is a big etiology of Membrano-proliferative GN?
hep B & C
40
LM of membrano-proliferative GN
hypercellular, hyperlobulated glomeruli leukocytes tran-tracking GBM deposits (C3)
41
EM membrane prolif
large subendo deposits
42
IF membrano proliferative
diffuse C3 deposits corresponding to lg immune complex
43
progonosis of membranoprolif
poor- end stage renal dx
44
lupus LM
6 classes--advances to nerotizing wire loop and lesions
45
EM lupus
extensive mesangial and maybe deposits everywhrre
46
IF lupus
"full house pattern"-everything, everywhere
47
3 types of hematuric GNitis
alport syndrome thin BM disease IgA Nephropathy (berger disease)
48
alport syndrome
nephritis with hematuria asociated with nerve deafness and ocular abnormalities
49
etio alport syndrome
sex-linked heterogenous group of mutations of collagen IV (a3 or 5) chain synthesis-->fragmentation of GBM
50
EM alport syndrome
fragmentation and splitting of GBM-->basket-weave pattern
51
thin basement diease
persistent or intemittent micro-hematuria (non-progressive, benign)
52
EM of thin BM disease
generalized thinning of BM
53
IgA nephropathy is the
commonest cause of GN worldwide
54
IgA nephro presentation
gross or microscopic hematuria (+ upper resp infx)
55
LM IgA
variable, but mainly mesangiprofiliferative
56
EM IGa and IG IgA
Iga deposits in mesangium
57
LM cresencitc disease
>50% of glomerular bowman's space is crescnet + compresse glomerular tuft + fibrin
58
IF+ cresenct
linear: anti GBM disease (ex- goodpasture) | granular- immune complex disease
59
IF- crescent
ANCA -:puaci-immune | ANCA+- systemic vasculatitis (wegners, churg strauss, microscopic polyangitis)

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