Non-inflammatory and Inflammatory Glomerular diseases Flashcards

1
Q

Nephritic Syndrome

A

Clinical presentation of inflammatory glomerulonephritis

  • Microscopic hematuria
  • Proteinuria
  • Hypertension
  • Edema
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2
Q

Nephrotic syndrome

A

Clinical presentation of non-inflammatory glomerulopathy

  • Proteinuria (>3.5g/d)
  • Hyperlipidemia
  • Edema
  • Hypoproteinemia
  • Urinalysis is key to diagnosis
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3
Q

Complications of nephrotic syndrome

A
  • Hypercoag
  • Edema
  • infection
  • Accelerated atherogenesis
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4
Q

Histopath of minimal change disease

A

Everything is normal (light, silver stain, immunofl) except electron microscopy which shows podocyte effacement

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5
Q

Etiology of minimal change disease

A

Unknown but can be secondary to NSAIDs or neoplasms

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6
Q

Treatment of minimal change disease

A

Steroids, podocytes look normal

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7
Q

Light micro: FSGS

A
  • Focal, segmental sclerosis
  • Segmental collapse with adhesions to bowman’s cap
  • Podocyte injury loss
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8
Q

Immunofl: FSGS

A

-IGM and C3 in collapsed mesangium

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9
Q

EM: FSGS

A

-Podocyte effacement, hyalin accumulation in cap loops–>collapse

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10
Q

Causes of FSGS

A

Podocyte injury leadin got proteinuria and glomerulosclerosis

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11
Q

What is the point of no return?

A

When about 40% of podocytes are lost, get global sclerosis

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12
Q

What attenuates podocyte loss and scarring?

A

RAAS inhibition

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13
Q

Why is podocyte injury so bad?

A

Don’t regenerate, leads to scarring and decreased GFR

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14
Q

Membranous glomerulopathy histology: PAS/silver stain

A

Sclerosis with basement membrane spikes

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15
Q

Membranous glomerulopathy histology: Trichrome

A

Sub epithelial proteinaceous deposits

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16
Q

Membranous glomerulopathy histology: Immunofl

A

IgG and C3 in the granular capillary loop

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17
Q

Membranous glomerulopathy histology: EM

A
  • Podocyte effacement
  • Subepi electron dense deposits
  • New BM surrounding immune complex deposits
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18
Q

Most common antibody found in membranous glomerulopathy?

A

M-type PLA2R

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19
Q

Secondary etiology of Membranous glomerulopathy

A
  • Infectious: Hep B, C, malaria etc
  • Neoplasms
  • Meds (gold salts, penicillamine)
  • Lupus
20
Q

What is glomerular inflammation a response to?

A

Final common response to capillary injury–>scar

21
Q

Steps of programmed response to capillary injury

A
  1. Holes/cap wall injury
  2. Proliferation (WBCs enter tufts)
  3. Acellular crescent formation (ECM fills bowman’s)
  4. Cellular crescent formation (cells in matrix produce scar)
  5. Glomerular and interstitial scarring
22
Q

Mechanisms that result in capillary injury?

A
  • Antibody mediated
  • Immune complex deposits
  • Mechanism X (vasculitis)
23
Q

Good pastures disesase

A

antibody mediated pulmonary-renal synrome with hemoptysis and RPGN

24
Q

Differential diagnosis for pulmonary-renal syndrome?

A

Good pastures, lupus, ANCA small v vasculitis

25
Q

Good pastures in light micro

A
  • Hypercellular glomerulus
  • Firbin
  • Crescents in bowman’s space
26
Q

Good pastures in immunofl

A
  • Linear GBM stain

- Stringy fibrin in bowman’s

27
Q

Good pastures in EM

A
  • Compressed glomerular tuft
  • Fibrin in bowman’s
  • No complexes
28
Q

Treatment of Good pastures

A
  • Plasma exchange
  • Immunosupp
  • Rituximab
29
Q

Post-strept GN

A

Immune complex mediated disease around 21 days post-strept with RPGN

30
Q

Post-strept GN light micro

A
  • Diffuse, proliferative exudative GN
  • Increased PNMs/glomerular cells
  • Occasional subepi deposits
  • Accentuated lobular structure
31
Q

Post-strept GN immunofl

A

Granular IgG, C3

32
Q

Post-strept GN EM:

A
  • large subepi deposits
  • no sclerotic rxn
  • subepi and mesangial deposits
33
Q

Lupus nephritis

A

Immune complex with RPGN, can also present with nephrotic syndrome

34
Q

Lupus nephritis Immunofl

A

“Full house pattern” stains for all

-granular cap and mesangial loop

35
Q

Lupus nephritis LM

A
  • Prolif in mesangium or lots of prolif everywhere
  • WIRE LOOPs=thick cap loops
  • Subendo deposits or epith
36
Q

Lupus nephritis EM

A
  • Mesangial, subepi and sub endo deposits

- Effaced podocytes

37
Q

IgA nephropathy

A

Immune complex disease that is slowly progressive with edema and gross hematuria (usually non-systemic)

38
Q

systemic version of IgA nephropathy

A

Henoch Schoenlein purpura (HSP)

  • Systemic vasculitis in childhood
  • RPGN, rash, colitis, arthritis
39
Q

IgA nephropathy light M

A
  • Hypercellularity in mesangium

- Focal crescents

40
Q

IgA nephropathy immunofl

A

Granular in mesang, igA and C3

41
Q

IgA nephropathy EM

A

Mesangial electron dense deposits

42
Q

ANCA-Associated SV Vasc

A

Pauci-immune GN (mech X) that mimics common diseases

43
Q

ANCA-Associated SV Vasc light M

A

Vasculitis with fibrinoid necrosis

necrotizing focal GN with crescents

44
Q

ANCA-Associated SV Vasc siver stain

A

focal crescents, segmental necrosis (loss of BM)

45
Q

ANCA-Associated SV Vasc Fl and EM?

A

None