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Nephrology Board Review Pearls > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

hypo-complementemic GNs

A
  • lupus GN
  • PIGN
  • cryoglobulinemic GN
  • MPGN
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2
Q

GNs with normal complements

A
  • IgA nephropathy
  • ANCA-associated GN
  • anti-GBM nephritis
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3
Q

GNs with granular pattern on IF

A
  • lupus GN
  • PIGN
  • cryoglobulinemic GN
  • MPGN
  • membranous nephropathy
  • IgA nephropathy
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4
Q

ONLY GN with LINEAR pattern on IF

A

anti-GBM nephritis

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5
Q

ONLY GN with pauci-immune pattern on IF

A

ANCA-associated GN

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6
Q

IgA nephropathy presentation

A
  • variable clinical presentation
  • asymptomatic hematuria with mild proteinuria
  • gross hematuria (sometimes with flank pain) within a FEW days of URI
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7
Q

mechanism of AKI in IgA nephropathy

A
  • crescentic IgA nephropathy

- tubular obstruction from erythrocytes

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8
Q

treatment of IgA nephropathy if proteinuria < 1 g/day

A

conservative therapy: ACEI/ARB, fish oil, vitamin d, and statin

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9
Q

treatment of IgA nephropathy if proteinuria > 1 g/day

A
  • conservative therapy: ACEI/ARB, fish oil, vitamin d, and statin
    IN ADDITION TO
  • steroids x 6 months
  • if crescentic (RPGN), ADD cyclophosphamide
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10
Q

LN classification

  • normal glomeruli on LM
  • mesangial immune deposits on IF
A

class 1; minimal mesangial LN

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11
Q

LN classification

  • purely mesangial hypercellularity of any degree or mesangial matrix expansion on LM
  • mesangial immune deposits
A

class 2; mesangial proliferative LN

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12
Q

LN classification

  • active or inactive focal, segmental or global
  • endo- or extracapillary GN involving < 50% of all glomeruli
  • typically with focal subendothelial immune deposits, with or without mesangial alterations
A

class 3; focal LN

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13
Q

LN classification

  • active or inactive focal, segmental or global
  • endo- or extracapillary GN involving > 50% of all glomeruli
  • typically with diffuse subendothelial immune deposits, with or without mesangial alterations
  • this class is subdivided into S (segmental) when 50% of involved glomeruli have segmental lesions, and G (global) when 50% of involved glomeruli have global lesions
A

class 4; diffuse LN

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14
Q

LN classification
- global or segmental subepithelial immune deposits or their morphologic sequelae on LM and on IF or EM, with or without mesangial alterations

A

class 5; membranous LN

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15
Q

histological prognostic features in LN

A
  • class 4 (diffuse proliferative LN)

  • high activity and chronicity on biopsy
  • crescents
  • interstitial fibrosis
  • segmental necrotizing lesions
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16
Q

clinical prognostic features in LN

A
  • HTN
  • anemia
  • high baseline Cr
  • high baseline proteinuria
  • delay in treatment
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17
Q

epidemiologic prognostic features in LN

A
  • black race

- low socioeconomic status

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18
Q

induction therapy of class 3 or class 4 LN with or without class 5 LN

A
  • steroids and cyclophosphamide (standard NIH protocol)
    OR
  • steroids and MMF (noninferior to CP)
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19
Q

maintenance therapy of class 3 or class 4 LN with or without class 5 LN

A

MMF

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20
Q

ANCA GN clinical presentation

- kidneys

A

brown, tea-colored urine

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21
Q

ANCA GN clinical presentation

- joints

A

pain and swelling

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22
Q

ANCA GN clinical presentation

- trachea and lungs

A
  • cough (often mistaken for PNA)
  • hemoptysis
  • dyspnea
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23
Q

ANCA GN clinical presentation

- skin

A
  • purpura
  • pruritus
  • hives
  • rash
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24
Q

ANCA GN clinical presentation

- sinus/nose

A
  • rhinorrhea
  • nose pain
  • nasal congestion
  • epistaxis
  • crusting of nares (poor prognostic factor indicative of relapse)
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25
Q

ANCA GN clinical presentation

- GIT

A
  • abdominal pain

- hematochezia/melena

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26
Q

ANCA GN clinical presentation

- eyes

A
  • eye pain
  • blurry vision
  • headache
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27
Q

ANCA GN clinical presentation

- ears

A
  • hearing loss
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28
Q

ANCA GN clinical presentation

- neuro

A

foot drop; mononeuritis multiplex

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29
Q

MC presenting symptom of ANCA

A

“I just don’t feel right”

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30
Q

vasculitis symptoms

A

flu-like symptoms including;

  • fever
  • body aches
  • poor appetite
  • weight loss
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31
Q

ANCA classification

A
  • renal limited vasculitis
  • microscopic polyangiitis (MPA)
  • granulomatosis with polyangiitis (GPA)
  • eosinophilic granulomatosis with polyangiitis (EGPA)
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32
Q

MCC of RPGN, especially as patients get older

A

ANCA-associated GN

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33
Q

better way to classify ANCA

A
  • renal-limited MPO-ANCA vasculitis
  • PR3-ANCA granulomatous vasculitis with lung 
and renal involvement 

  • MPO-ANCA necrotizing vasculitis with 
multi-organ involvement 

  • pauci-immune, necrotizing glomerulonephritis 
in setting of positive MPO-ANCA
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34
Q

induction therapy for ANCA GN

A
  • pulse steroids for everyone (taper at 8 weeks)
  • plasmapheresis (everyone with pulmonary hemorrhage or “severe” renal failure)
  • cyclophosphamide or rituximab
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35
Q

maintenance therapy for ANCA GN

A
  • azathioprine
    OR
  • rituximab
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36
Q

goal to come off steroids in treatment of ANCA vasculitis by what time frame?

A

6 months

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37
Q

treatment for ANCA GN relapse

A

rituximab

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38
Q

“DOUBLE positive” ANCA serologies with very high titers for anti-MPO should raise suspicion for

A

drug-induced ANCA vasculitis

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39
Q

drugs that can cause lupus

A
  • procainamide
  • hydralazine
  • minocycline
  • diltiazem
  • penicillamine
  • isoniazid
  • quinidine
  • anti-TNF alpha therapy
  • methyldopa
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40
Q

drugs that can cause ANCA

A
  • hydralazine
  • levamisole (cocaine contaminant)
  • propylthiouracil (PTU)
  • minocycline
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41
Q

MCC of chronic GN worldwide

A

IgA nephropathy

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42
Q

other common cause of acute and chronic GN

A

LN

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43
Q

crescentic GN on LM, and linear pattern on IF

A

anti-GBM nephritis

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44
Q

anti-GBM nephritis with lung involvement

A

Goodpasture’s disease (pulmonary-renal involvement)

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45
Q

epidemiology of anti-GBM nephritis

A
  • bimodal age and gender
  • young MEN in 2nd and 3rd decade
  • OLDER WOMEN in 6th and 7th decade
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46
Q

up to 1/3 of patients with anti-GBM nephritis have concurrent

A

ANCA, usually MPO

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47
Q

prognosis of anti-GBM

A
  • very poor

- must be diagnosed and treated early

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48
Q

anti-GBM treatment

A
  • plasmapheresis daily until anti-GBM Ab cleared
  • pulse steroids then taper over 6 months
  • cyclophosphamide (PO is better) x 3 months
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49
Q

does anti-GBM relapse?

A

very rarely; considered to be “one and done”

50
Q

should you f/u anti-GBM after treatment and how?

A
  • yes!

- anti-GBM titers

51
Q

PIGN key clinical features

A
  • occurs after acute infection
  • classic nephritic picture with microscopic or gross hematuria
  • AKI
  • proteinuria
  • HTN
  • edema
  • VERY LOW C3
  • low/normal C4
52
Q

PIGN is more common in

A

children

53
Q

causative agents of PIGN

A
  • Staphylococcus becoming more common

- Streptococcus

54
Q

PIGN key LM findings

A
  • diffuse ENDOcapillary proliferative GN

- crescents in severe cases

55
Q

PIGN key IF findings

A

“STARRY SKY” pattern; GRANULAR deposits in capillary walls and mesangium with C3 staining +/- IgG

56
Q

PIGN key EM findings

A

SUBepithelial hump-shaped deposits

57
Q

classical complement pathway consumption is triggered by

A

immune complexes (Ag and Ab)

58
Q

if classical complement pathway is triggered what is expected on IF?

A

C3 and Ab staining, such as IgG

59
Q

if you ONLY see C3 staining on IF then you can assume what?

A

alternative complement pathway was triggered

60
Q
  • LM; mesangial proliferation with mesangial interposition and GBM duplication
  • IF; C3 with IgG and/or IgM, C1
A

MPGN type 1

61
Q
  • diverse glomerular histology w/ or w/o MPGN pattern

- C3 alone

A

C3 glomerulopathy (previously MPGN type 2)

62
Q

types of C3 glomerulopathy

A
  • C3 GN (MPGN type 1 pattern)
  • DDD
  • C3 GN (MPGN type 3 pattern)
63
Q
  • LM; mesangial proliferation with mesangial interposition and GBM duplication, usually with MEMBRANOUS features
  • IF; C3 with IgG and/or IgM, C1
A

MPGN type 3

64
Q

classical complement pathway triggered by what conditions?

A
  • infection
  • cancer
  • autoimmune disease
  • allergic reaction
65
Q

alternative complement pathway HYPERACTIVITY triggered by

A
  • mutations
  • auto-Abs
  • monoclonal gammopathy
66
Q

possible treatment for C3 glomerulopathy that targets C5

A

eculizumab

67
Q

name the 4 possible HCV related GNs

A
  • type 1 MPGN a/w type 2 cryoglobulinemia
  • MPGN without cryoglobulinemia (probably false negative d/t difficulty checking cryoglobulins)
  • membranous nephropathy
  • FSGS, TMA a/w anti-cardiolipin Ab, fibrillary GN, and immunotactoid GN
68
Q

how many types of cryoglobulins are there?

A

3

69
Q

cryoglobulinemia

  • type 1
  • what IGs and type?
A

MONOclonal IgG, IgM, or IgA

70
Q

cryoglobulinemia

  • type 1
  • a/w what diseases?
A

lymphoproliferative d/o’s; MM, WM, CLL, B-cell NHL

71
Q

cryoglobulinemia

  • type 2
  • what IGs and type?
A
  • MONOclonal IgM, IgM, or IgA with RF activity
    OR
  • POLYclonal IgG
72
Q

cryoglobulinemia

  • type 2
  • a/w what diseases?
A
  • infections, mainly HCV
  • autoimmune d/o’s
  • lymphoproliferative d/o’s
  • rarely idiopathic
73
Q

cryoglobulinemia

  • type 3
  • what IGs and type?
A

POLYclonal mixed IGs (all isotypes) with RF activity from one polyclonal component (usually IgM)

74
Q

cryoglobulinemia

  • type 3
  • a/w what diseases?
A
  • infections, mainly HCV
  • autoimmune d/o’s
  • rarely idiopathic
75
Q

RF is only positive in which types of cryoglobulinemia?

A

types 2 and 3

76
Q

hallmark LM and EM findings of cryoglobulinemia

A
  • LM = MPGN, nodular pattern

- EM = precipitating cryoglobulins in glomerulus

77
Q

hallmark laboratory features of HCV-cryoglobulinemic GN

A
  • variable proteinuria
  • hematuria
  • renal insufficiency
  • LOW C4, sometimes low C3
  • RF positive (if type 2 or 3)
  • elevated transaminases in 70%
78
Q

treatment of HCV-associated cryoglobulinemic MPGN

  • IF mild to moderate proteinuria
  • IF slow but progressive loss of kidney function
  • IF eGFR > 50
A

interferon + ribavirin +/- protease inhibitor

79
Q

treatment of HCV-associated cryoglobulinemic MPGN

  • IF mild to moderate proteinuria
  • IF slow but progressive loss of kidney function
  • IF eGFR < 50
A

interferon ONLY

80
Q

treatment of HCV-associated cryoglobulinemic MPGN

  • IF nephrotic range proteinuria
  • IF rapidly progressive loss of kidney function
A
  • plasmapheresis x 2-3 weeks
  • rituximab x 4 weeks or CP x 2-4 months
  • pulse steroids +/- taper
  • after controlling acute vasculitis, treat HCV
81
Q

definition of hemolytic-uremic syndrome

A
  • microangiopathic hemolytic anemia (MAHA)
  • thrombocytopenia
  • AKI
82
Q

expected laboratory findings of microangiopathic hemolytic anemia (MAHA)

A
  • schistocytes on PBS
  • elevated LDH
  • low haptoglobin
  • elevated bilirubin
83
Q

90% of HUS is typical, which means what?

A
  • caused by Shiga-like toxin

- prodromal episode of diarrhea

84
Q

10% of HUS is “atypical,” which means what?

A
  • heterogeneous d/o
  • NO diarrhea
  • NO Shiga toxin-producing E. coli infection
85
Q

classification of atypical HUS

A 
# familial
# sporadic:
- idiopathic
- pregnancy-associated
- HELLP syndrome
- drug-induced
- organ transplantation
- HIV
# cancer
86
Q

most common protein affected by genetic abnormalities in patients with aHUS

A

factor H

87
Q

treatment for aHUS

A

plasmapheresis then eculizumab

88
Q

eculizumab works by targeting

A

C5

89
Q

Alport syndrome defect in

A

type 4 collagen α-5 chain gene (COL4A5)

90
Q

most common GN inherited by X-linked pattern

A

Alport syndrome

91
Q

can Alport syndrome be inherited by AR or AD pattern?

A

yes

92
Q

clinical presentation of Alport syndrome

A
  • microscopic hematuria
  • subnephrotic range proteinuria
  • declining renal function
  • sensorineural hearing loss
  • anterior lenticonus of eye
93
Q

diagnosis of Alport syndrome if NO ESTABLISHED family history

A

renal biopsy

94
Q

renal biopsy findings of Alport syndrome

A

EM required***

  • GBM THICKENING
  • lamellation –> “BASKET-WEAVE” appearance
95
Q

diagnosis of Alport syndrome if POSITIVE family history

A

GENETIC TESTING for α3, α4, and α5 chains of type 4 collagen

96
Q

epidemiology of Alport syndrome

A

MALE predominance

97
Q

thin basement membrane nephropathy renal biopsy findings

A 
# EM required***
- diffuse GBM ATTENUATION (thinning)
98
Q

epidemiology of thin basement membrane nephropathy

A
  • familial (often), or sporadic

- no gender difference

99
Q

thin basement membrane nephropathy presentation

A
  • microscopic hematuria

- NORMAL renal function

100
Q

thin basement membrane nephropathy AKA

A

benign familial hematuria

101
Q

thin basement membrane nephropathy caused by

A

COL4A3 or COL4A4 gene mutation

102
Q

GNs a/w subENDOthelial deposits

A
  • MPGN type 1
  • MPGN type 3
  • cryoglobulinemia
  • LN class 3
  • LN class 4
103
Q

GNs a/w double contours (same list as GNs a/w subENDOthelial deposits + 2 more)

A
  • MPGN type 1
  • MPGN type 3
  • cryoglobulinemia
  • LN class 3
  • LN class 4
  • TMA
  • chronic transplant glomerulopathy
104
Q

diffuse thinning of GBM

A

thin basement membrane disease

105
Q

irregularity and multilayering or splitting of the GBM

A

Alport’s syndrome

106
Q

diffuse thickening of the GBM

A
  • diabetic nephropathy
  • hypertensive nephrosclerosis
  • Alport’s disease
107
Q

mainly IgG LINEAR deposition in capillary walls

A

anti-GBM disease

108
Q

nonspecific LINEAR IgG or “PSEUDOLINEAR” IgG deposition in capillary walls

A

diabetic nephropathy

109
Q

GRANULAR parietal deposition of IGs and COMPLEMENT

- subENDOthelial

A

MPGN type 1

110
Q

GRANULAR parietal deposition of IGs and COMPLEMENT

- subEPIthelial

A

PIGN

111
Q

GRANULAR parietal deposition of IGs and COMPLEMENT

- subENDOthelial AND intramembranous

A

membranous GN

112
Q

what Ab in granulomatosis with polyangiitis ANCA?

A

anti-PR3 ANCA

113
Q

what Ab eosinophilic granulomatosis with polyangiitis ANCA?

A

anti-MPO ANCA

114
Q

ONLY GN with granular pattern on IF AND NORMAL complements

A

IgA nephropathy

115
Q

GRANULAR parietal deposition of IGs and COMPLEMENT

- subENDOthelial, subEPIthelial, AND intramembranous

A

MPGN type 3

116
Q

“SAUSAGE-LIKE” (ribbon-like), osmiophilic deposits

- GBM deposits

A

DDD

117
Q

GN a/w Drusen bodies in retina

A

DDD (C3 deposition in retina)

118
Q
  • MPGN pattern LM
  • negative IF
  • GBM deposits with ribbon-like pattern
A

DDD

119
Q

treatment for DDD

A

eculizumab

120
Q
  • MPGN pattern LM
  • negative IF
  • subENDOthelial AND mesangial deposits
A

C3 GN

121
Q

treatment for C3 GN

A

rituximab and plasmapheresis

Nephrology Board Review Pearls (10 decks)

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