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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
Q
A

HSP

mesangial deposit and subendothelial deposit

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26
Q

clinical signs of SLE

A

highly variable, nephritis, nephrotic syndrome, renal failure, often hypocomplementemic most common in young black females

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27
Q

pathology of SLE

A

variable, 6 different patterns, class 3 and 4 show focal and diffuse hypercellularity, tuft necrosis, crescents, usually presents with nephritis; membranous pattern

IF - full house (IgG, IgM, IgA, C3, C1q)

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28
Q

pathogenesis of SLE

A

autoimmunity-antigens include DNA, RNA, nucleoproteins

29
Q
A

focal lupus nephritis class 3

30
Q
A

diffuse lupus nephritis class 4

31
Q
A

SLE

full house

32
Q
A

SLE

immune deposits, subepithelial and subendothelial deposits

33
Q
A

tubuloreticular inclusion

SLE

34
Q

what is MPGN

A

a pattern of injury more than one particular disease

35
Q

clinical characteristics of MPGN

A

nephrotic and nephritic

hypocomplementemia; often progresses to chronic renal failure

36
Q

pathology of MPGN

A

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
Q

pathogenesis of MPGN

A

Ig+ - antigen excess, secondary to infection (HCV, HBV)

Ig- - C3 glomefrulonephritis/dense deposit, abnormal alternative complement activation (genetic or acquired)

38
Q

what is NeFa

A

autoantibody that stabilizes C3 convertase. A defect associated with MPGN

39
Q
A

MPGN

lobular hypercellularity

40
Q
A

MPGN

double contours

41
Q
A

MPGN

C3 deposits
Ig-

42
Q
A

MPGN

Subendothelial deposits

double contour

43
Q
A

MPGN

DDDz

44
Q

clinical scenarios of goodpastures

A

RPGN, alpha GBM mediated pulmonary renal vasculitic syndrome

most have both lung and renal development

45
Q

pathology of goodpastures sydnrome

A

light microscopy - crescentic GN; affects capillaries, NO arterial involvement

IF - shows linear IgG in GBM

EM - necrosis, endothelial and subendothelial swelling, no deposits

46
Q

pathogenesis of goodpastures

A

autoantibody, antigen is alpha 3 chain of type 4 collagen in the non collangenous globular domain (COL4A3)

47
Q
A

goodpastures

48
Q
A

goodpastures

49
Q

ANCA associated renal disease causes

A

Wegners (GPA)

MPA - microscopic polyangiitis

churg strUSS (EGPA)

ANCA associate GN

50
Q

clinicla presentation of GPA

A

RPGN

systemic vasculitis, no asthma, granulomas, upper airway commonly affected

51
Q

MPA clinical scenario

A

RPGN

systemic vasculitis

pulmonary involved but NO asthma, no granulomas

52
Q

EGPA clinical scenario

A

RPGN, asthma, eosinophilia, granulomas

53
Q

clinical presentation of ANCA associated GN

A

RPGN, no systemic vasculitis

54
Q

GPA anca

A

75% cANCA/PR3

20% pANCA/MPO

55
Q

MPA ANCA status

A

40% cANCA

50% pANCA

56
Q

EGPA ANCA status

A

60% pANCA

57
Q

ANCA status of ANCA-GN

A

70% pANCA

58
Q

ANCA associated renal disease light, IF, EM

A

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
Q
A

ANCA associated renal disease

60
Q
A

ANCA associated renal disease

61
Q

alport syndrome clinical dx

A

hematuria, proteinuria, chronic progressice renal failure, x linked heritable, deafness, ocular cataracts

62
Q

pathology of alport syndrome

A

variable; alternative thinning, thickening and splitting of capillary basement membranes seen by EM

63
Q

pathophys of alport

A

X linked - 80% defectivec collagen biosynthesis

5 chain of type 4 collagen COL4A5

AR - 15% COL4A3 or COL4A4 (chrom 2)

64
Q
A

alport syndrome

65
Q
A

alport syndrome

66
Q

clinical features of benign recurrent hematuria

A

microscopic or macroscopic hematuria; generally indolent course

67
Q

pathology of benign recurrent hematuria

A

generally only minor abnormalities; diffuse thinning of glomerular basement membranes seen by electron microscopy

68
Q

pathyphys of benign recurrent hematuria

A

autosomal dominant

mutation in COL4A3, COL4A4 in about 40%

69
Q
A

benign recurrent hematuria

GIR Test 3 (6 decks)

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