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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

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

A

Low C3, but normal C4 - Demonstrates alternative pathway activation

18
Q

Suggested pathogenesis of Focal Segmental Glomerulosclerosis

A

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

19
Q

What causes Spike and Dome appearance

A

Subepithelial deposits with thin tracts of new GBM separating the deposits

20
Q

Which subtype of Focal Segmental Glomerulosclerosis has a rapid onset of nephrotic syndrome with rapid progression to renal failure

A

Collapsing Glomerulopathy

20
Q

What is hyalinosis in FSGS

A

Accumulation of leaked plasma protiens and lipids

22
Q

What causes 75% of nephrotic syndrome cases in children

A

Minimal Change Disease

23
Q

Soluble Urokinase-type plasminogen activator receptor (suPAR) is elevated in serum of 2/3 of patients with

A

Focal Segmental Glomerulosclerosis

23
Q

Tx of FSGS

A

Corticosteroids (poor response) and Calcineurin inhibitors

26
Q

LM histology of Focal Segmental Glomerulosclerosis

A

Scarring, Adhesions to bowman’s capsule, Occluded cap lumens, Hyalinosis

27
Q

The Collapsing Glomerulopathy subtype of FSGS is often associated with

A

HIV infection or drug toxicity

28
Q

suPAR binds to and activates

A

Beta3-integrin, a major podocyte-anchoring protein

29
Q

Prognosis of Minimal Change Disease

A

Resolves with steroid tx in >90% of kids; Response slow in adults; Recurrence is common

31
Q

Minimal change disease causes about__ of nephrotic cases in children

A

75%

32
Q

What mutation in AA’s confers 10.5-fold higher incidence of Focal Segmental Glomerulosclerosis

A

ApoL1

34
Q

5 features accompanying Nephrotic Syndrome that indicate FSGS over MCD

A

Older Age, Hematuria, HTN, Non-selective Proteinuria, Poor response to steroids

35
Q

Probably pathogenic mechanism causing most cases of Primary Membranous Nephropathy

A

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

37
Q

Ages of minimal change disease

A

Very young or very old

38
Q

Presentation of Membranous Nephropathy

A

Most with nephrotic syndrome, rest with asymptomatic proteinuria

40
Q

Most common subtype of Focal Segmental Glomerulosclerosis

A

Not Otherwise Specified

41
Q

Demographic of Membranous Nephropathy

A

Caucasian Male Adults

42
Q

EM of Membranous Nephropathy

A

Effacement of FP’s and Spike and Dome: Subepithelial deposits with tracks of BM separating them

43
Q

Top two findings in FSGS

A

Nephrotic Range Proteinuria, Hematuria

44
Q

LM of Post-Strep GN

A

Diffuse proliferative GN, prominent endocapillary proliferation and numerous neutrophils

44
Q

NEP is the target antigen in

A

Congenital Membranous nephropathy

46
Q

m-type PLA2

A

Immune complexes –> Most primary Membranous Nephropathy

48
Q

LM, IF, and EM of Minimal Change Disease

A

LM and IF are negative, but EM shows foot process effacement

49
Q

Post-Strep GN typically presents with

A

Nephritic Syndrome

50
Q

Tea or Cola Colored Urine

A

Post-Infectious GN

52
Q

Why is it important to differentiate FSGS from MCD

A

Prognosis is much worse in FSGS

53
Q

PLA2R is the target antigen in

A

Primary (idiopathic) Membranous Nephopathy

54
Q

EM of Post-Strep GN

A

Subepithelial electron-dense deposits = Humps

55
Q

Insidious onset of Nephrotic Syndrome in child with good response to steroid tx

A

Minimal Change Disease

56
Q

Cornerstone of tx in Minimal Change Disease

A

Oral Glucocorticoids

57
Q

What causes podocyte injury in Membranous Nephropathy

A

Formation of MAC due to auto-Ab binding (to m-type PLA2R)

58
Q

Time fram of Post-Strep GN after infection

A

1-6 weeks

Renal (31 decks)

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