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Renal > 05.14 - Nephrotic Syndrome 2 (Nichols, Showkat) - PP + Handout > Flashcards

05.14 - Nephrotic Syndrome 2 (Nichols, Showkat) - PP + Handout Flashcards

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1
Q

suPAR

A

Binds Beta3-integrin –> FSGS

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1
Q

Reduce __ is associated with secondary FSGS

A

Reduced nephron mass

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2
Q

Chronic, slowly progressive disease wih GBM thickening, Subepithelial immune complex deposits, and effacement of foot processes

A

Membranous Nephropathy

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2
Q

IF of Post-Strep GN

A

Diffuse granular deposts of IgG and C3

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2
Q

Prognosis of Post-Strep GN

A

Generally good in children; 40% of adults develop chronic azotemia

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2
Q

ApoL1 mutation makes you susceptible to

A

FSGS

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3
Q

AI w/ immune complexes formed in situ from binding of filtered auto-ab to podocyte m-type PLA2R

A

Probably pathogenic mechanism causing most cases of Primary Membranous Nephropathy

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4
Q

IF in MCD and FSGS are usually both

A

negative

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5
Q

Role of suPAR, beta3-integrin, and podocytes in Focal Segmental Glomerulosclerosis

A

suPAR binds to and activates beta3-integrin, a major podocyte anchoring protein

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5
Q

EM of Focal Segmental Glomerulosclerosis

A

Effacement of foot processes

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5
Q

If poor response to steroids in MCD, think of

A

Unsampled focal segmental glomerulosclerosis

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5
Q

Why is effacement of foot process likely mediated by MAC

A

Intermediary chemotactic fragments, C3a and C5a, are washed away into urinary space

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6
Q

Demographic of Post-Strep GN

A

School age children, male preponderance

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7
Q

LM of Membranous Nephropathy

A

Thickening of GBM

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9
Q

Most common demographic of Focal Segmental Glomerulosclerosis

A

Adult black males

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10
Q

Why no inflammation in Membranous Nephropathy

A

Complement not activated b/c at a site that is not in contact with circulating inflammatory cells

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11
Q

Most common cause of Nephortic Syndrome in Caucasian Adults

A

Membranous Nephropathy

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11
Q

Thickened GBM w/out increased cellularity

A

Membranous Nephropathy

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12
Q

Most common cause of Nephrotic Syndrome in Black Adults

A

64% Focal Segmental Glomerulosclerosis

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13
Q

IF of FSGS

A

Normal

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14
Q

Membranous Nephropathy vs Post-Infectious GN: Which is nephritic and which nephrotic

A

Membranous Nephropathy is nephrotic

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15
Q

Diffuse endocapillary proliferation and infiltration by numerous neutrophils

A

Post-Strep GN

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16
Q

IF of Membranous Nephropathy

A

Granular subepithelial deposits of IgG and Complement

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17
Q

Complement changes in Post-Strep GN

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A

Low C3, but normal C4 - Demonstrates alternative pathway activation

18
Suggested pathogenesis of Focal Segmental Glomerulosclerosis
suPAR binds to and activates beta3-integrin, a major podocyte anchoring protein
19
What causes Spike and Dome appearance
Subepithelial deposits with thin tracts of new GBM separating the deposits
20
Which subtype of Focal Segmental Glomerulosclerosis has a rapid onset of nephrotic syndrome with rapid progression to renal failure
Collapsing Glomerulopathy
20
What is hyalinosis in FSGS
Accumulation of leaked plasma protiens and lipids
22
What causes 75% of nephrotic syndrome cases in children
Minimal Change Disease
23
Soluble Urokinase-type plasminogen activator receptor (suPAR) is elevated in serum of 2/3 of patients with
Focal Segmental Glomerulosclerosis
23
Tx of FSGS
Corticosteroids (poor response) and Calcineurin inhibitors
26
LM histology of Focal Segmental Glomerulosclerosis
Scarring, Adhesions to bowman's capsule, Occluded cap lumens, Hyalinosis
27
The Collapsing Glomerulopathy subtype of FSGS is often associated with
HIV infection or drug toxicity
28
suPAR binds to and activates
Beta3-integrin, a major podocyte-anchoring protein
29
Prognosis of Minimal Change Disease
Resolves with steroid tx in \>90% of kids; Response slow in adults; Recurrence is common
31
Minimal change disease causes about\_\_ of nephrotic cases in children
75%
32
What mutation in AA's confers 10.5-fold higher incidence of Focal Segmental Glomerulosclerosis
ApoL1
34
5 features accompanying Nephrotic Syndrome that indicate FSGS over MCD
Older Age, Hematuria, HTN, Non-selective Proteinuria, Poor response to steroids
35
Probably pathogenic mechanism causing most cases of Primary Membranous Nephropathy
AI w/ immune complexes formed in situ from binding of filtered auto-ab to podocyte m-type PLA2R
37
Ages of minimal change disease
Very young or very old
38
Presentation of Membranous Nephropathy
Most with nephrotic syndrome, rest with asymptomatic proteinuria
40
Most common subtype of Focal Segmental Glomerulosclerosis
Not Otherwise Specified
41
Demographic of Membranous Nephropathy
Caucasian Male Adults
42
EM of Membranous Nephropathy
Effacement of FP's and Spike and Dome: Subepithelial deposits with tracks of BM separating them
43
Top two findings in FSGS
Nephrotic Range Proteinuria, Hematuria
44
LM of Post-Strep GN
Diffuse proliferative GN, prominent endocapillary proliferation and numerous neutrophils
44
NEP is the target antigen in
Congenital Membranous nephropathy
46
m-type PLA2
Immune complexes --\> Most primary Membranous Nephropathy
48
LM, IF, and EM of Minimal Change Disease
LM and IF are negative, but EM shows foot process effacement
49
Post-Strep GN typically presents with
Nephritic Syndrome
50
Tea or Cola Colored Urine
Post-Infectious GN
52
Why is it important to differentiate FSGS from MCD
Prognosis is much worse in FSGS
53
PLA2R is the target antigen in
Primary (idiopathic) Membranous Nephopathy
54
EM of Post-Strep GN
Subepithelial electron-dense deposits = Humps
55
Insidious onset of Nephrotic Syndrome in child with good response to steroid tx
Minimal Change Disease
56
Cornerstone of tx in Minimal Change Disease
Oral Glucocorticoids
57
What causes podocyte injury in Membranous Nephropathy
Formation of MAC due to auto-Ab binding (to m-type PLA2R)
58
Time fram of Post-Strep GN after infection
1-6 weeks

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