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Step 1 > Glomerular Disease Details > Flashcards

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
Q

Diffuse proliferative GN IF

A

Granular

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26
Q

IgA Nephropathy (Berger DZ) presentation

A
  • Childhood
  • Episodic gross hematuria that occurs concurrently with respiratory or GI tract infections (IgA is secreted by mucosal lining)
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27
Q

What condition is IgA Nephropathy (Berger DZ) associated with?

A

Henoch-Schonlein Purpura (GI, kidneys, skin, joints)

28
Q

IgA Nephropathy (Berger DZ) LM

A

Mesangial proliferation

29
Q

IgA Nephropathy (Berger DZ) EM

A

Mesangial IC depositis

30
Q

IgA Nephropathy (Berger DZ) IF

A

IgA based IC deposits in mesangium

31
Q

Alport Syndrome presentation?

A 
Eye problems (retinopathy, lens dislocation) + glomerulonephritis + sensorineural deafness
\+ Family hx
32
Q

Alport Syndrome pathogenesis

A

Mutation in type IV collagen –> thinning and splitting (lamellated) of glomerular BM

33
Q

Hereditary pattern of Alport Syndrome?

A

X-linked dominant

34
Q

Alport Syndrome EM?

A

“Basket weave” appearance

35
Q

Membranoproliferative glomerulonephritis presentation?

A

Nephritic syndrome that often copresents with nephrotic syndrome

36
Q

Type I MPGN associations?

A

Hepatitis B or C

37
Q

Type I MPGN Pathology

A
  • SUBENDOTHELIAL IC deposits
  • Granular IF
  • “tram track” on PAS stain due to GBM splitting caused by mesangial ingrowth
38
Q

Type II MPGN associations?

A

C3 nephritic factor –> stabilizes C3 convertase –> decreased serum C3 levels

39
Q

What is Type II MPGN also called?

A

Dense deposit disease

40
Q

Characteristics of nephrotic syndrome?

A

Massive proteinuria with hypoalbuminemia –> edema, hyperlipidemia (blood becomes thin so liver increases fat)
- Frothy urine with fatty casts

41
Q

What is nephrotic syndrome caused by?

A

Podocyte damage –> disrupts glomerular filtration charge barrier

42
Q

Why is nephrotic syndrome associated with hypercoagulable state?

A

Pee out ATIII in urine

43
Q

What is nephrotic syndrome associated with infection?

A

Pee out Ig in urine

44
Q

Presentation of minimal change disease (liphoid nephrosis)?

A
  • KIDS
  • Idiopathic
  • Triggered by recent infection, immunization, immune stimulus
  • May be secondary to lymphoma (CK-mediated damage)
45
Q

Minimal change disease LM

A

NORMAL glomeruli

46
Q

Minimal change disease IF

A

Negative

47
Q

Minimal change disease EM

A

Effacement of foot processes due to CKs

48
Q

Describe the proteinuria of Minimal change disease?

A

Selective (loss of Alb but not Ig)

49
Q

Treatment of minimal change disease?

A

Excellent response to steroids

50
Q

Focal Segmental Glomerulosclerosis presentation?

A 
AA and hispanics
Idiopathic
HIV
Sickle Cell
Heroin abuse
Massive obesity
Interferon treatment
Chronic kidney disease due to congenital malformations
51
Q

Focal Segmental Glomerulosclerosis LM

A

Segmental sclerosis and hyalinosis

52
Q

Focal Segmental Glomerulosclerosis IF

A

Often negative

May be positive for nonspecific focal deposits of IgM, C3, C1

53
Q

Focal Segmental Glomerulosclerosis EM

A

Effacement of foot processes

54
Q

Focal Segmental Glomerulosclerosis treatment?

A

Inconsistent response to steroids, may progress to chronic renal disease

55
Q

Membranous Nephropathy (Membranous GN) presentation?

A

Caucasian adults
Primary - Ab to phospholipase A2 R
Secondary - drugs (NSAIDs, penicillamine), infections (HBV, HCV), SLE, or solid tumors

56
Q

Membranous Nephropathy LM

A

Diffuse capillary and GBM thickening

57
Q

Membranous Nephropathy IF

A

Granular as a result of IC deposition (nephrotic presentation of SLE)

58
Q

Membranous Nephropathy EM

A

“Spike and dome” appearance with subepithelial deposits

59
Q

Membranous Nephropathy treatment?

A

Poor response to steroids, may progress to chronic renal disease

60
Q

Diabetic Glomerulonephropathy presentation?

A

Diabetes w/ proteinuria

61
Q

Pathogenesis of Diabetic Glomerulonephropathy?

A
  • Nonenzymatic glycosylation of GBM –> increased permeability, thickening
  • Nonenzymatic glycosylation of efferent arterioles –> increase in GFR –> mesangial expansion –> hyaline arteriosclerosis
  • Microalbuminuria
62
Q

What is the most common cause of end-stage renal disease in the U.S.?

A

Diabetic Glomerulonephropathy

63
Q

Diabetic Glomerulonephropathy LM?

A

Mesangial expansion
GBM thickening
Eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)

64
Q

Diabetic Glomerulonephropathy treatment?

A

Ace inhibitor - blocks Ang II –> decrease P at efferent arteriole –> decrease rate of injury

65
Q

Buzzwords for Diabetic Glomerulonephropathy

A

HYALINE ARTERIOSCLEROSIS

KIMMELSTIEL-WILSON LESIONS

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