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Renal > Nephrotic Syndrome 2 > Flashcards

Nephrotic Syndrome 2 Flashcards

1
Q

What are the 2 podoctyopathies?

A

minimal change disease and focal segmental glomerulosclerosis

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2
Q

Who usually gets minimal change disease?

A

very young and very old - bimodal distribution

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3
Q

What is the most common cause of nephrotic syndrome in kids?

A

minimal change disease

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4
Q

What other clinical findings are common in minimal change disease?

A
  1. insidious onset of edema
  2. normal blood pressure
  3. usually normal renal function
  4. highly selective proteinuria - albumin
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5
Q

What is thought to be the pathogenesis for minimal change disease?

A

not clear but thought to be mediated by a T cell that secretes a circulating permeability factor that causes podocyte damage

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6
Q

What is seen w/ minimal change disease for pathology?

A

effacement and detachment of foot processes

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7
Q

What is the treatment for minimal change disease?

A

oral glucocorticoids

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8
Q

Who responds well to steriods in minimal change disease?

A

kids

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9
Q

If there is a poor response to steroids what should be done?

A
  1. look for other cause (especially in children)

2. unsampled focal segmental glomerulosclerosis

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10
Q

What are some clinical findings for focal segmental glomerulosclerosis?

A
  1. high BP

2. low albumin –> proteinuria

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11
Q

How many of the pts w/ focal segmental glomerulosclerosis develop end stage kidney disease?

A

50%

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12
Q

What is Supar?

A

the circulating factor that binds to beta2 integrin and causes effacement of podocytes

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13
Q

What are some secondary causes of focal segmental glomerulosclerosis?

A
  1. familial – mutation in genes alpha-actinin-4, podosin, TRCP6, and APOL1
  2. infection - HIV or Parvo virus
  3. drugs - pamidronate, heroin, Li
  4. Loss of nephron mass
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14
Q

Why are people of African descent susceptible to getting focal segmental glomerulosclerosis?

A

b/c 40% of them have mutations in APOL1 making them susceptible to African sleeping sickness

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15
Q

Why does hyalinosis occur in FSG?

A

accumulation of leaked plasma proteins and lipids

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16
Q

T or F. Adhesion of involved segment to Bowman Capsule does occur in FSG?

A

T

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17
Q

What are subtypes of FSG?

A
  1. collapsing
  2. cellular
  3. tip
  4. Perhiliar
  5. not otherwise specified (42%)
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18
Q

Which of the subtypes of FSG will most likely obtain remission?

A

Tip

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19
Q

What is found in the collapsing type of FSG?

A

collapsed BM and adhesions common

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20
Q

What shows up on immunofluoresence for FSG?

A

nothing really

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21
Q

What is the treatment for FSG?

A

sterois and immunosuppressive

22
Q

what immunosuppressive drugs are used for FSG?

A

calcinuerin inhibitors – cyclosporine and tacrolimus

23
Q

What is steroid sensitivity for FSG?

A
  1. Steroid Sensitive - proteinuria remits w/ treatment and means good prognosis
  2. Sterois resistant - proteinuria persists and means bad prognosis
24
Q

What happens to repeated relapses of Minimal change disease in children w/ steroid responsive nephrotic syndrome?

A

may develops into FSG secondar to repreated renal injury

25
Q

What is the filtered cationic Ag formation of membranous nephropathy?

A

deposits from circulation cross endothelium and GBM and localize in the subepithelial spaces, then Abs localize and cause nephritis

26
Q

What is the Autoimmunity model of in-situ formation of membranous nephropathy (MN)?

A

locally generated Ag and filtered AutoAb

27
Q

What are examples of autoimmunity model?

A
  1. M-type Phospholipase A2 Recepto (PLA2R) – Primary MN

2. Neutral endopeptidase (NEP) - target Ag in congentical MN

28
Q

How is PLA2R involved in primary MN?

A
  • expressed by podocytes in normal human glomeruli

- found to be co-localized w/ IgG4 in immune deposits in glomeruli of patients w/ idiopathic MN

29
Q

What are some secondary diseases taht MN is associated w/?

A
  1. infection - Hep B, syphilis, Malaria
  2. Autoimmune - SLE
  3. Drugs - Gold, penicillamine, captopril, NSAID
  4. Malignancy - lung cancer, colon cancer, melanoma
30
Q

What is the most common cause of nephrotic syndrome in Caucasian adults?

A

Membranous nephropathy

31
Q

What is the epidemiology of MN?

A
  • peaks in 4th to 6th decades

- males commonly affected

32
Q

What happens to pts w/ MN?

A
  1. spontaneous resolution in 30%
  2. progressive renal failure in 40%
  3. presistent proteinuria w/ variable renal dysfuntion in 30%
33
Q

What are risk factors for loss of renal function in MN?

A
  1. male
  2. > 10g/24 hrs of proteinuria
  3. HTN
  4. Azotemia
  5. Tubulointerstitial fibrosis
  6. glomerulosclerosis
34
Q

What do you see on light microscopy for MN?

A

thickened BM w/out increased cellularity

35
Q

What do you see w/ immunofluorescence in MN?

A

granular deposits of IgG and complement

36
Q

What would you see on electron microscopy for MN?

A

diffusely thickened BM w/ subepithelial deposits separated by spikes of new GBM –> spike and dome pattern

37
Q

Is there inflammation found in MN?

A

no – remember it’s nephrotic! complement that you see is activated at a site that is not in contact w/ circulating inflammatory cells

38
Q

What happens if MN is secondary to another disease?

A

resolution of subepithelial depotis is slow w/ concomitant slow resolution of proteinuria – up to 2 yrs

39
Q

What is the likely mechanism for the retraction and effacement of podocyte foot processes in subepithelial deposits?

A

-complement dependent process mediated by MAC and intermediary chemotactic fragments are washed away into urinary space

40
Q

What are the clinical findings w/ post-infectious glomerulonephritis? (PIGN)

A
  • usually associated w/ recent infection
  • gross hematuria
  • HTN common
  • signs of fluid retention –peripheral edema, ascites
  • proteinuria
  • impaired renal function
41
Q

What are the lab result findings for PIGN?

A
  • low C3 and C4
  • elevated anti-streptolysin O titers if preceded by throat infection
  • elevated anti-DNAse B titers if preceded by skin infection
  • positive blood culture in sepsis
42
Q

What is seen on light microscopy for PIGN?

A
  • diffuse endocapillary proliferation and infiltration by numerous PMNS
43
Q

What is seen on immunofluorescence for PIGN?

A

diffuse grandular deposits in capillary walls and mesangium (IgG and C3)

44
Q

What is seen on EM for PIGN?

A

subepithelial humps

45
Q

What are supportive measures for PIGN?

A
  • control HTN w/ antihypertensives and diuretics
  • renal replacement therapy if sever kidney dysfunction
  • treat infection
46
Q

How long does it take to resolve the HTN?

A

a few weeks

47
Q

How long to get normal C3 levels

A

6 wks

48
Q

how long to resolve hematuria

A

w/in 12 months

49
Q

Summary – What is seen w/ the different kidney biopsies for minimal change disease?

A

LM- normal
Immuno - normal
EM - podocyte foot process fusion

50
Q

Summary – What is seen w/ the different kidney biopsies for focal segmental glomerulosclerosis?

A
  • LM - scarring and adhesion to Bowman’s Capsule
  • Immuno - normal
  • EM - podocyte foot process fusion
51
Q

Summary – What is seen w/ the different kidney biopsies for MN?

A

LM - diffuse thickening of glomerular BM w/ normal cellularity
Immuno - fine granular w/ IgG and complement
EM - subepithelial deposits

52
Q

Summary – What is seen w/ the different kidney biopsies for PIGN?

A

LM- proliferation , inflammation
Immuno- granular deposition of C3 and IgG
EM - subepithelial humps

Renal (33 decks)

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