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Renal > 05.14 - Nephritic Syndrome (Nichols, Hastings) - PP + Handout > Flashcards

05.14 - Nephritic Syndrome (Nichols, Hastings) - PP + Handout Flashcards

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1
Q

2 Podocyte Disorders

A

Minimal Change Disease, Focal Segmental Glomerulosclerosis

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2
Q

3 basic components of Nephritic Sydnrome

A

Hematuria, Renal Insufficiency, HTN

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3
Q

3 GBM Diseases

A

Anti-GBM Disease, Alport’s, Thin BM Disease

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4
Q

Ab’s to ___ occur in about 80% of patients with DDD

A

C3 Nephritic Factor

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5
Q

Accumulation and proliferation of cells outside the glomerular tuft which can result in compression of the tuft

A

Crescents

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6
Q

Age of MPGN presentation

A

older children and younger adults (7-30)

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7
Q

Anti-GBM Disease is characterized by

A

Auto-Ab’s against epitope in non-collagenous domain of alpha 3 type 4 collagen

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8
Q

As a general principal, MPGN is usually ___ in children, and ___ in adults

A

Primary in children, secondary in adults

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9
Q

Auto-Ab’s against epitope in non-collagenous domain of alpha 3 type 4 collagen

A

Anti-GBM Disease is characterized by

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10
Q

Berger’s Disease is aka

A

IgA Nephropathy

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11
Q

BM in Alport Syndrome

A

Abnormally thin, with splintering of lamina densa causing basket weave appearance

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12
Q

Buzz word for Alport Syndrome

A

Basket Weave

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13
Q

C3 deposition on IF, electron-dense deposits on EM

A

IF and EM of DDD

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14
Q

C3 levels in MPGN 1 vs DDD

A

Low in both

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15
Q

C3 Nephritic Factor

A

80% of DDD cases

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16
Q

Characeteristic feature of IgA Nephropathy

A

Deposition of IgA1 in MM

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17
Q

Characteristic double contour resembling tram tracks on silver stain

A

MPGN

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18
Q

Characteristic LM manifestation in glomeruli of RPGN

A

Crescents in Bowman’s space

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19
Q

Clinical manifestation of Endothelial Damage

A

Hematuria

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20
Q

Correlation between anti-gbm titers and disease activity

A

None

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21
Q

Crescentic infiltration causes proliferation of

A

Mononuclear cells and Parietal Epithelial Cells

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22
Q

Crescents in RPGN are composed of

A

proliferating parietal epithelial cells, macrophages, fibrin; eventually areas of necrosis

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23
Q

Crucial feature of Type 3 RPGN

A

Negative IF

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24
Q

DDD is differentiated from other forms of GN

A

EM: Ribbons of dense, dark material deposited w/in GBM

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25
DDD is not caused by \_\_\_, but instead by dysregulation of \_\_\_
Not by immune complexes, by dysregulation of complement system
26
Demographic of Anti-GBM disease
Young white males
27
Demography of IgA Nephropathy
East Asian male children
28
EM of DDD
Ribbons of dense, dark material deposited w/in GBM
29
Endothelial cell injury in glomerular capillaries can lead to
Thrombus formation
30
Glomerular endothelial cell injury and capillary thrombus formation can occur in absence of immune complexes and cause a syndrome called
Thrombotic Microangiopathy
31
Heterozygous females in X-Linked Alport Syndrome
May have hematuria and thin BM
32
Histology of Anti-GBM disease
Crescentic necrotizing GN, w/ characteristic linear deposits of IgG along GBM
33
How are granular deposits in Type 2 RPGN visualized
EM
34
How are linear deposits in Type 1 RPGN visualrized
IF
35
How soon after infection will you see nephritic sediment in IgA Nephropathy
Synpharyngitic: 1-2 Days
36
IF and EM of DDD
C3 deposition on IF, electron-dense deposits on EM
37
IgA Nephropathy differs from post-strep GN in being
Synpharyngitic
38
IgA Nephropathy has immune complex deposition in what location
Mesangial location
39
IgA Nephropathy is differentiated from other forms of GN by
IF: characterstic findings of mesangial IgA deposits, often with C3 and properdin
40
IgA Nephropathy is typcially triggered by
URTI or GI infection
41
IgA Nephropathy results in ___ pattern of injury
Mesangioproliferative
42
Incidence of IgA Nephropathy is increased in patients with
Celiac Disease or Chronic Liver Disease (decreased hepatobiliary clearance)
43
Is crescent formation due to antibodies or a cell-mediated process
Can be either
44
Is RPGN a medical emergency
No, but requires prompt dx and tx
45
It is thought that DDD is a ___ disease, that becomes manifest when \_\_\_
Two-Hit, infection or autoimmunity gives rise to excess of immune complexes or complement activation
46
Location of MPGN Deposits
Subendothelial
47
Lupus nephritis immune complex deposition tends to occur in what location
Subendothelial
48
Macular deposits in the eyes and/or acquired partial lipodystrophy
DDD
49
Mesangial proliferation in MPGN is likely in response to
Circulating immune complexes
50
Most common MPGN type
Type 1 (80%)
51
Most common primary GN worldwide
IgA Nephropathy
52
MPGN diseases have LM appearance combining
Thickened, split GBM w/ a proliferation of glomerular cells and infiltration of inflammatory cells
53
MPGN has immune complex deposition in what location
Subendothelial
54
Mutation in Alport Syndrome
Alpha5 chain of Type 4 collagen
55
One of the most common diseases to have the nephritic-nephrotic phenotype
MPGN
56
Other notable location of Dense Deposits in DDD
Bruch membrane of eye
57
Pathogenesis of IgA Nephropathy
Aberrant Glycosylation of O-linked glycans in the hinge region of IgA1
58
Patients with Anti-GBM disease who have pulmonary and renal involvement
Goodpasture's Syndrome
59
Plasmapharesis in Type 2 RPGN
not helpful
60
Post-infectious GN immune complex deposition tends to be in what location
Subepithelial
61
Presentation of Anti-GBM
Nephritic syndrome, Heamturia, rapid renal failure
62
Prognosis in DDD
Poor
63
Prognosis of Anti-GBM disease
Poor - Rapid progressive GN
64
Prognosis of Type 1 MPGN
Poor, slow progression to ESRD requiring dialysis or transplant
65
Progression to Fibrous Crescents
Segmental proliferative and necrotizing lesions --\> Cellular Crescents --\> Fibrocellular crescents --\> Fibrous Crescents
66
Renal Insuff can be manifested by
Oliguria and/or Azotemia
67
Ribbons of dense dark material within GBM on EM
DDD
68
RPGN can be characterized by
Type of Glomerular deposits
69
RPGN with Granular (immune complex) deposits
Primary renal disease, secondary renal disease
70
RPGN with linear glomerular deposits
Anti-GMB disease, Goodpasture
71
RPGN with no glomerular deposits
Drug-induced, Idiopathic, ANCA-associated (wegener's or Micrscopic Poly)
72
Secondary MPGN can be a complication of
Hep C
73
Single most characteristic feature of Nephritic Syndrome
Hematuria
74
Systemic form of IgA Nephropathy
Henoch-Schonlein Purpura
75
Triad of Alport Syndrome
Nephritis, Nerve Deafness, and Lens disorders (all need defective collagen)
76
Tx of Anti-GBM disease
Plasmapharesis, Steroids, Immunosuppressives
77
Tx of IgA Nephropathy
Steroids, ACEi's, ARB's
78
Type 1 MPGN is mediated by \_\_\_, causing activation of \_\_\_\_\_
Immune complexes, activaiton of complement by classical pathway
79
Type 2 RPGN can be seen in severe cases of
Post-Strep GN, Lupus Nephritis, and IgA Nephropathy
80
Type 2 RPGN: in addition to crescents, there is
segmental necrosis, mesangial cell proliferation, and exudate w/ leukocytes
81
Uniform reduction in GBM to about 1/2 of normal thickness
Thin Basement Membrane Disease
82
What are recruited by damaged endothelial cells in MPGN
Monocytes and Macrophages
83
What causes tram track appearance
Formation of new BM and entrapment of immune complexes, complement factors, cellular elements, and matrix material
84
What differentiates MPGN 1 from DDD in IF
MPGN 1 has C3 and IgG, but DDD has just C3
85
What does IF show in Type 1 MPGN
Granular deposits of C3 and IgG
86
What frequently precedes the kidney diesease in Dense Deposit Disease
URTI
87
What frequently precedes the kidney disease in Type 1 MPGN
URTI
88
What glomerular disease is often associated with Hep C infection
MPGN 1
89
What is abundantly increased in MPGN
Mesangial Matrix
90
What is the basket weave
Alport: GBM has several alternating layers of lamina rar and lamina densa
91
What type of immune complex deposition is injurious to endothelial cells
Subendothelial
92
Where are IgA complexes primarily deposited in IgA Nephropathy
Mesangium
93
Where are immunce complexes formed in MPGN? IgA Nephropathy? Lupus?
Outside, outside, outside
94
Where is new BM formed in MPGN
At the mesangial cell - endothelial cell interface
95
Which complement pathway is dysregulated in DDD
Alternative

Renal (31 decks)

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