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GIR Test 3 > B5.046 - Pathology of Kidney Glomerular Disease Pt 2 > Flashcards

B5.046 - Pathology of Kidney Glomerular Disease Pt 2 Flashcards

1
Q

clinical indications for biopsy

A

nephrotic syndrome

nephritis

asymptomatic hematuria

acute renal failure

chronic renal failure

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2
Q

what is nephritis

A

hematuria, mild-mod proteinuria, HTN, increased SCr, active urine sediment

RBCs dysmorphic RBC casts in urine

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3
Q
A

dysmorphic RBCs in nephritic syndrome

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4
Q
A

RBC casts

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5
Q

what is RPGN

A

a type of nephritis

characterized by rapid loss of renal fxn, typically 50% loss of GFR within days up to 3 months

may be a/w nephrotic proteinuria

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6
Q

morphologic correlate of RPGN

A

glomerular crescent formation

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7
Q

3 types of RPGN

A

type 1 - anti GBM

2 - immune complex GN

3 - anti neutrophil cytoplasmic antibody (ANCA associated)

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8
Q

causes of nephritis

A
  1. post infectious glomerulonephritis
  2. IgA nephrophathy
  3. lupus nephritis
  4. membranoproliferative glomerulonephritis
  5. goodpastures
  6. ANCA associated glomerulonephritis
  7. hereditary nephritis (alports)
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9
Q

PIGN features

A

hypocomplementemia, hematuria, proteinuria, decline in GFR

infxn with GAS is classic

most common in kids/YA

delay in symptoms 1-4 wks, (1-2 wk throat, 3-6 wk skin)

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10
Q

light, IF, EM of PIGN

A

light - variable, usually diffuse endocapillary hypercellularity, including PMNs; crecents

IF: IgG, C3 (granular, starry sky) GBM pattern; mesangial later in course

EM: subepithelial humps

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11
Q
A

PIGN note the hypercellularity

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12
Q
A

PIGN, IgG, C3 GBM pattern

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13
Q
A

PIGN

subepithelial humps

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14
Q

clinical presentation of IgA nephropathy

A

recurrent hematuris, often associated with simultaneous URI, may progress to chronic renal failure; most common in young white males in US v common among asians

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15
Q

pathology of IgA nephropathy

A

mesangial expansion/cellular proliferation

immunoflorescence: classically mesangial IgA, C3

EM: mesangial/paramesangial deposits

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16
Q
A

IgA nephropathy

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17
Q
A

IgA nephropathy

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18
Q
A

IgA nephropathy

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19
Q

causes of 2nd degree IgA nephropathy

A

GI dz: celica, UC, crohns, liver dz

autoimmune: AS, RA, psoriasis, Reiters, behcets

Infx: HIV, TB, campylobacter

neoplastic

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20
Q

HSP presentation

A

nephritis

rash

arthritis

abdominal pain

most common in children

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21
Q

HSP pathology

A

glomeruli: mesangial expansion/proliferation, often with necrosis; crescents are common but rarely exceed 50% of gloms; can have endocapillary proliferation

IF: diffuse granular IgA dominant deposits

EM: mesangial, subendothelial deposits

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22
Q

how do you distinguish HSP from IgAN

A

clinical history required

HS usually has crescents and subendothelial deposits by EM

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23
Q
A

HSP

crescent, matrix expansion, hypercellularity

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24
Q
A

HSP

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25
HSP mesangial deposit and subendothelial deposit
26
clinical signs of SLE
highly variable, nephritis, nephrotic syndrome, renal failure, **often hypocomplementemic** most common in young black females
27
pathology of SLE
variable, 6 different patterns, class 3 and 4 show focal and diffuse hypercellularity, tuft necrosis, crescents, usually presents with nephritis; membranous pattern IF - f**ull house (IgG, IgM, IgA, C3, C1q)**
28
pathogenesis of SLE
autoimmunity-antigens include DNA, RNA, nucleoproteins
29
focal lupus nephritis class 3
30
diffuse lupus nephritis class 4
31
SLE full house
32
SLE immune deposits, subepithelial and subendothelial deposits
33
tubuloreticular inclusion SLE
34
what is MPGN
a pattern of injury more than one particular disease
35
clinical characteristics of MPGN
nephrotic and nephritic hypocomplementemia; often progresses to chronic renal failure
36
pathology of MPGN
2 types Ig+ and Ig- both show diffuse intrinsic **lobular hypercellularity; double contours or tram tracks** IF - usually peripheral C3 EM - subendothelial deposits or intramembranous dense deposits
37
pathogenesis of MPGN
Ig+ - **antigen excess**, secondary to infection **(HCV, HBV)** Ig- - **C3 glomefrulonephritis/dense deposit,** abnormal **alternative complement activation** (genetic or acquired)
38
what is NeFa
autoantibody that stabilizes C3 convertase. A defect associated with MPGN
39
MPGN lobular hypercellularity
40
MPGN double contours
41
MPGN C3 deposits Ig-
42
MPGN Subendothelial deposits double contour
43
MPGN DDDz
44
clinical scenarios of goodpastures
RPGN, alpha GBM mediated pulmonary renal vasculitic syndrome most have both lung and renal development
45
pathology of goodpastures sydnrome
light microscopy - crescentic GN; affects capillaries, NO arterial involvement IF - **shows linear IgG** in GBM EM - necrosis, endothelial and subendothelial swelling, no deposits
46
pathogenesis of goodpastures
autoantibody, antigen is alpha 3 chain of type 4 collagen in the non collangenous globular domain (COL4A3)
47
goodpastures
48
goodpastures
49
ANCA associated renal disease causes
Wegners (GPA) MPA - microscopic polyangiitis churg strUSS (EGPA) ANCA associate GN
50
clinicla presentation of GPA
RPGN systemic vasculitis, no asthma, granulomas, upper airway commonly affected
51
MPA clinical scenario
RPGN systemic vasculitis pulmonary involved but NO asthma, no granulomas
52
EGPA clinical scenario
RPGN, asthma, eosinophilia, granulomas
53
clinical presentation of ANCA associated GN
RPGN, no systemic vasculitis
54
GPA anca
75% cANCA/PR3 20% pANCA/MPO
55
MPA ANCA status
40% cANCA 50% pANCA
56
EGPA ANCA status
60% pANCA
57
ANCA status of ANCA-GN
70% pANCA
58
ANCA associated renal disease light, IF, EM
light - **necrotizing crecentic glomerulonephritis,** periglomerular inflammation, leukocytoclastic angiitis (arteries, arterioles) IF - non specific trapping, **"pauci immune"** EM - necrosis, endothelial and subendothelial swelling use combo of clinical and path features to make specific dx
59
ANCA associated renal disease
60
ANCA associated renal disease
61
alport syndrome clinical dx
**hematuria**, proteinuria, chronic progressice renal failure, x linked heritable, **deafness, ocular cataracts**
62
pathology of alport syndrome
variable; alternative thinning, thickening and splitting of capillary basement membranes seen by EM
63
pathophys of alport
**X linked - 80%** defectivec collagen biosynthesis 5 chain of type **4 collagen COL4A5** **AR - 15%** COL4A3 or COL4A4 (chrom 2)
64
alport syndrome
65
alport syndrome
66
clinical features of benign recurrent hematuria
microscopic or macroscopic hematuria; generally indolent course
67
pathology of benign recurrent hematuria
generally only **minor abnormalities;** diffuse thinning of glomerular basement membranes seen by electron microscopy
68
pathyphys of benign recurrent hematuria
autosomal dominant mutation in **COL4A3, COL4A4 in about 40%**
69
benign recurrent hematuria

GIR Test 3 (6 decks)

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