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Renal > Glomerular Disease > Flashcards

Glomerular Disease Flashcards

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
Q

tests for FSGS

A

LM: segmental collapse ins caring in SOME glomeruli
EM: effacement foot processes, thick BM
IF: - except some IgM/C3 trapping

25
Q

FSGS etiology

A

can be either idiopathic (suPAR) or secondary (family, adaptive, viruses (parvo, hiv), drugs (heroin, lithium)

26
Q

evolution of membranous glomeruopathy

A

immune complex deposits accumulate—>GBM reacts by forming spike like projects–>grow to spike and dome–>lead to thickened basement membranes

27
Q

MG is the main cause of nephrotic syndrome in

A

adults

28
Q

etiology of MGNopathy

A

primary and secondary (drugs, tumors, lupus, infx)

29
Q

tests and MGpathy

A

LM: suepithelial immune deposits
EM-subepithelial spike like projects of GBM
IF: diffuse GRANULAR pattern–Igg, c3

30
Q

LM of diabetes early and late

A

early: glomerular hypertrophy, widened sclerotic mesangium, thickend GBM
advanced progressive GBM thickening with KW spots, microaneurysms, arteriolar hylinization

31
Q

EM for diabetes

A

thick GBM

mesangial sclerosis

32
Q

IF for diabetes

A

neg for deposits

33
Q

LM for amyloidosis

A

mesangial and GBM deposition of b pleated amyloid

congo red!

34
Q

EM amyloidosis

A

8-12 fibrils

35
Q

IF amyloidosis

A

negative, but lambda chain positive

36
Q

LM acute post-infectious GN

A

diffuse endocapi. prolif with LEUKOCYTES

swollen, hypercellular glomerulus

37
Q

EM APIG

A

hump like deposits

38
Q

IF APIG

A

granular along GBM (c3!)

39
Q

what is a big etiology of Membrano-proliferative GN?

A

hep B & C

40
Q

LM of membrano-proliferative GN

A

hypercellular, hyperlobulated glomeruli
leukocytes
tran-tracking
GBM deposits (C3)

41
Q

EM membrane prolif

A

large subendo deposits

42
Q

IF membrano proliferative

A

diffuse C3 deposits corresponding to lg immune complex

43
Q

progonosis of membranoprolif

A

poor- end stage renal dx

44
Q

lupus LM

A

6 classes–advances to nerotizing wire loop and lesions

45
Q

EM lupus

A

extensive mesangial and maybe deposits everywhrre

46
Q

IF lupus

A

“full house pattern”-everything, everywhere

47
Q

3 types of hematuric GNitis

A

alport syndrome
thin BM disease
IgA Nephropathy (berger disease)

48
Q

alport syndrome

A

nephritis with hematuria asociated with nerve deafness and ocular abnormalities

49
Q

etio alport syndrome

A

sex-linked heterogenous group of mutations of collagen IV (a3 or 5) chain synthesis–>fragmentation of GBM

50
Q

EM alport syndrome

A

fragmentation and splitting of GBM–>basket-weave pattern

51
Q

thin basement diease

A

persistent or intemittent micro-hematuria (non-progressive, benign)

52
Q

EM of thin BM disease

A

generalized thinning of BM

53
Q

IgA nephropathy is the

A

commonest cause of GN worldwide

54
Q

IgA nephro presentation

A

gross or microscopic hematuria (+ upper resp infx)

55
Q

LM IgA

A

variable, but mainly mesangiprofiliferative

56
Q

EM IGa and IG IgA

A

Iga deposits in mesangium

57
Q

LM cresencitc disease

A

> 50% of glomerular bowman’s space is crescnet + compresse glomerular tuft + fibrin

58
Q

IF+ cresenct

A

linear: anti GBM disease (ex- goodpasture)

granular- immune complex disease

59
Q

IF- crescent

A

ANCA -:puaci-immune

ANCA+- systemic vasculatitis (wegners, churg strauss, microscopic polyangitis)

Renal (17 decks)

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