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Glomerular Disease Details Flashcards

1
Q

Signs of glomerulonephritis

A

RBC casts!

Axotemia, oliguria, HTN, proteinuria

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2
Q

Acute Poststreptococcal GN Presentation

A
  • KIDS
  • 2-4 wks after Group A strep infection of pharynx or skin
  • Peripheral or periorbital edema, cola-colored urine, HTN
  • Positive strep titers/serologies, decreased complement levels due to consumption
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3
Q

Acute Poststreptococcal GN LM

A

Glomeruli enlarged and hypercellular

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4
Q

Acute Poststreptococcal GN IF

A 
"Starry sky"
Granular appearance ("lumpy bumpy")
Due to IgG, IgM, and C3 deposition along GBM and mesangium
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5
Q

Acute Poststreptococcal GN EM

A

SUBEPITHELIAL IC humps

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6
Q

Acute Poststreptococcal GN Treatment

A

Usually resolves spontaneously, supportive rx

  • Kids rarely progress to renal failure
  • Some adults develop RPGN - only 60% of adult cases resolve completely (increased age –> poor px)
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7
Q

What type of HSN rxn is Acute Poststreptococcal GN?

A

Type III (Ab-Ag complexes)

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8
Q

Presentation of Rapidly Progressive (Crescentic) Glomerulonephritis

A
  • Rapidly deteriorating renal function

- Poor px

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9
Q

Disease proceses that result in Rapidly Progressive (Crescentic) Glomerulonephritis?

A
  • Goodpasture
  • Granulomatosis with polyangiitis (Wegener)
  • Microscopic polyangiitis
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10
Q

Presentation of Goodpasture?

- RPGN

A

Hematuria and hemoptysis

YA male

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11
Q

Type of HSN rxn is Goodpasture?

- RPGN

A

Type II HSN rxn (cytotoxic Ab mediated)

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12
Q

Pathogenesis of Goodpasture?

- RPGN

A

Ab to GBM and alveolar basement membrane (type IV collagen)

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13
Q

Goodpasture IF

- RPGN

A

Linear

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14
Q

Goodpasture Treatment

- RPGN

A

Emergent plasmapheresis

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15
Q

Presentation of Wegener’s?

- RPGN

A

Nasopharynx + lungs + kidneys

Middle aged male

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16
Q

Wegener’s IF?

- RPGN

A

Negative (pauci-immune)

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17
Q

Wegener’s markers?

- RPGN

A

PR3-ANCA/c-ANCA (anti-proteinase 3)

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18
Q

Microscopic polyangiitis presentation

- RPGN

A

Lungs + kidneys + palpable purpura
NO nasopharyngeal involvement
NO granulomas

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19
Q

Microscopic polyangiitis IF

- RPGN

A

Negative (pauci-immune)

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20
Q

Microscopic polyangiitis marker

- RPGN

A

MPO-ANCA/p-ANCA (anti-myeloperoxidase)

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21
Q

Rapidly Progressive (Crescentic) Glomerulonephritis LM and IF?

A
  • Cresent moon shape - consist of FIBRIN and plasma proteins (C3b) with glomerular parietal cells, monocytes, and MACS
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22
Q

Diffuse proliferative GN caused by?

A

SLE (common CoD)

Membranoproliferative glomerulonephritis

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23
Q

Diffuse proliferative GN LM

A

“wire looping” of capillaries

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24
Q

Diffuse proliferative GN EM

A

SUBENDOTHELIAL and sometimes intramembranous IgG-based ICs

Often with C3 deposition

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25
Diffuse proliferative GN IF
Granular
26
IgA Nephropathy (Berger DZ) presentation
- Childhood - Episodic gross hematuria that occurs concurrently with respiratory or GI tract infections (IgA is secreted by mucosal lining)
27
What condition is IgA Nephropathy (Berger DZ) associated with?
Henoch-Schonlein Purpura (GI, kidneys, skin, joints)
28
IgA Nephropathy (Berger DZ) LM
Mesangial proliferation
29
IgA Nephropathy (Berger DZ) EM
Mesangial IC depositis
30
IgA Nephropathy (Berger DZ) IF
IgA based IC deposits in mesangium
31
Alport Syndrome presentation?
``` Eye problems (retinopathy, lens dislocation) + glomerulonephritis + sensorineural deafness + Family hx ```
32
Alport Syndrome pathogenesis
Mutation in type IV collagen --> thinning and splitting (lamellated) of glomerular BM
33
Hereditary pattern of Alport Syndrome?
X-linked dominant
34
Alport Syndrome EM?
"Basket weave" appearance
35
Membranoproliferative glomerulonephritis presentation?
Nephritic syndrome that often copresents with nephrotic syndrome
36
Type I MPGN associations?
Hepatitis B or C
37
Type I MPGN Pathology
- SUBENDOTHELIAL IC deposits - Granular IF - "tram track" on PAS stain due to GBM splitting caused by mesangial ingrowth
38
Type II MPGN associations?
C3 nephritic factor --> stabilizes C3 convertase --> decreased serum C3 levels
39
What is Type II MPGN also called?
Dense deposit disease
40
Characteristics of nephrotic syndrome?
Massive proteinuria with hypoalbuminemia --> edema, hyperlipidemia (blood becomes thin so liver increases fat) - Frothy urine with fatty casts
41
What is nephrotic syndrome caused by?
Podocyte damage --> disrupts glomerular filtration charge barrier
42
Why is nephrotic syndrome associated with hypercoagulable state?
Pee out ATIII in urine
43
What is nephrotic syndrome associated with infection?
Pee out Ig in urine
44
Presentation of minimal change disease (liphoid nephrosis)?
- KIDS - Idiopathic - Triggered by recent infection, immunization, immune stimulus - May be secondary to lymphoma (CK-mediated damage)
45
Minimal change disease LM
NORMAL glomeruli
46
Minimal change disease IF
Negative
47
Minimal change disease EM
Effacement of foot processes due to CKs
48
Describe the proteinuria of Minimal change disease?
Selective (loss of Alb but not Ig)
49
Treatment of minimal change disease?
Excellent response to steroids
50
Focal Segmental Glomerulosclerosis presentation?
``` AA and hispanics Idiopathic HIV Sickle Cell Heroin abuse Massive obesity Interferon treatment Chronic kidney disease due to congenital malformations ```
51
Focal Segmental Glomerulosclerosis LM
Segmental sclerosis and hyalinosis
52
Focal Segmental Glomerulosclerosis IF
Often negative | May be positive for nonspecific focal deposits of IgM, C3, C1
53
Focal Segmental Glomerulosclerosis EM
Effacement of foot processes
54
Focal Segmental Glomerulosclerosis treatment?
Inconsistent response to steroids, may progress to chronic renal disease
55
Membranous Nephropathy (Membranous GN) presentation?
Caucasian adults Primary - Ab to phospholipase A2 R Secondary - drugs (NSAIDs, penicillamine), infections (HBV, HCV), SLE, or solid tumors
56
Membranous Nephropathy LM
Diffuse capillary and GBM thickening
57
Membranous Nephropathy IF
Granular as a result of IC deposition (nephrotic presentation of SLE)
58
Membranous Nephropathy EM
"Spike and dome" appearance with subepithelial deposits
59
Membranous Nephropathy treatment?
Poor response to steroids, may progress to chronic renal disease
60
Diabetic Glomerulonephropathy presentation?
Diabetes w/ proteinuria
61
Pathogenesis of Diabetic Glomerulonephropathy?
- Nonenzymatic glycosylation of GBM --> increased permeability, thickening - Nonenzymatic glycosylation of efferent arterioles --> increase in GFR --> mesangial expansion --> hyaline arteriosclerosis - Microalbuminuria
62
What is the most common cause of end-stage renal disease in the U.S.?
Diabetic Glomerulonephropathy
63
Diabetic Glomerulonephropathy LM?
Mesangial expansion GBM thickening Eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)
64
Diabetic Glomerulonephropathy treatment?
Ace inhibitor - blocks Ang II --> decrease P at efferent arteriole --> decrease rate of injury
65
Buzzwords for Diabetic Glomerulonephropathy
HYALINE ARTERIOSCLEROSIS | KIMMELSTIEL-WILSON LESIONS

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