Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Nephrology Board Review Pearls > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

(121 cards)

Start Studying
1
Q

hypo-complementemic GNs

A
  • lupus GN
  • PIGN
  • cryoglobulinemic GN
  • MPGN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

GNs with normal complements

A
  • IgA nephropathy
  • ANCA-associated GN
  • anti-GBM nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

GNs with granular pattern on IF

A
  • lupus GN
  • PIGN
  • cryoglobulinemic GN
  • MPGN
  • membranous nephropathy
  • IgA nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ONLY GN with LINEAR pattern on IF

A

anti-GBM nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ONLY GN with pauci-immune pattern on IF

A

ANCA-associated GN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

mechanism of AKI in IgA nephropathy

A
  • crescentic IgA nephropathy

- tubular obstruction from erythrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

treatment of IgA nephropathy if proteinuria < 1 g/day

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

LN classification

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

class 1; minimal mesangial LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

clinical prognostic features in LN

A
  • HTN
  • anemia
  • high baseline Cr
  • high baseline proteinuria
  • delay in treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

epidemiologic prognostic features in LN

A
  • black race

- low socioeconomic status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

MMF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ANCA GN clinical presentation

- kidneys

A

brown, tea-colored urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ANCA GN clinical presentation

- joints

A

pain and swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ANCA GN clinical presentation

- trachea and lungs

A
  • cough (often mistaken for PNA)
  • hemoptysis
  • dyspnea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ANCA GN clinical presentation

- skin

A
  • purpura
  • pruritus
  • hives
  • rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ANCA GN clinical presentation

- sinus/nose

A
  • rhinorrhea
  • nose pain
  • nasal congestion
  • epistaxis
  • crusting of nares (poor prognostic factor indicative of relapse)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
ANCA GN clinical presentation | - GIT
- abdominal pain | - hematochezia/melena
26
ANCA GN clinical presentation | - eyes
- eye pain - blurry vision - headache
27
ANCA GN clinical presentation | - ears
- hearing loss
28
ANCA GN clinical presentation | - neuro
foot drop; mononeuritis multiplex
29
MC presenting symptom of ANCA
"I just don't feel right"
30
vasculitis symptoms
flu-like symptoms including; - fever - body aches - poor appetite - weight loss
31
ANCA classification
- renal limited vasculitis - microscopic polyangiitis (MPA) - granulomatosis with polyangiitis (GPA) - eosinophilic granulomatosis with polyangiitis (EGPA)
32
MCC of RPGN, especially as patients get older
ANCA-associated GN
33
better way to classify ANCA
- 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
34
induction therapy for ANCA GN
- pulse steroids for everyone (taper at 8 weeks) - plasmapheresis (everyone with pulmonary hemorrhage or "severe" renal failure) - cyclophosphamide or rituximab
35
maintenance therapy for ANCA GN
- azathioprine OR - rituximab
36
goal to come off steroids in treatment of ANCA vasculitis by what time frame?
6 months
37
treatment for ANCA GN relapse
rituximab
38
"DOUBLE positive" ANCA serologies with very high titers for anti-MPO should raise suspicion for
drug-induced ANCA vasculitis
39
drugs that can cause lupus
- procainamide - hydralazine - minocycline - diltiazem - penicillamine - isoniazid - quinidine - anti-TNF alpha therapy - methyldopa
40
drugs that can cause ANCA
- hydralazine - levamisole (cocaine contaminant) - propylthiouracil (PTU) - minocycline
41
MCC of chronic GN worldwide
IgA nephropathy
42
other common cause of acute and chronic GN
LN
43
crescentic GN on LM, and linear pattern on IF
anti-GBM nephritis
44
anti-GBM nephritis with lung involvement
Goodpasture's disease (pulmonary-renal involvement)
45
epidemiology of anti-GBM nephritis
- bimodal age and gender - young MEN in 2nd and 3rd decade - OLDER WOMEN in 6th and 7th decade
46
up to 1/3 of patients with anti-GBM nephritis have concurrent
ANCA, usually MPO
47
prognosis of anti-GBM
- very poor | - must be diagnosed and treated early
48
anti-GBM treatment
- plasmapheresis daily until anti-GBM Ab cleared - pulse steroids then taper over 6 months - cyclophosphamide (PO is better) x 3 months
49
does anti-GBM relapse?
very rarely; considered to be "one and done"
50
should you f/u anti-GBM after treatment and how?
- yes! | - anti-GBM titers
51
PIGN key clinical features
- occurs after acute infection - classic nephritic picture with microscopic or gross hematuria - AKI - proteinuria - HTN - edema - VERY LOW C3 - low/normal C4
52
PIGN is more common in
children
53
causative agents of PIGN
- Staphylococcus becoming more common | - Streptococcus
54
PIGN key LM findings
- diffuse ENDOcapillary proliferative GN | - crescents in severe cases
55
PIGN key IF findings
"STARRY SKY" pattern; GRANULAR deposits in capillary walls and mesangium with C3 staining +/- IgG
56
PIGN key EM findings
SUBepithelial hump-shaped deposits
57
classical complement pathway consumption is triggered by
immune complexes (Ag and Ab)
58
if classical complement pathway is triggered what is expected on IF?
C3 and Ab staining, such as IgG
59
if you ONLY see C3 staining on IF then you can assume what?
alternative complement pathway was triggered
60
- LM; mesangial proliferation with mesangial interposition and GBM duplication - IF; C3 with IgG and/or IgM, C1
MPGN type 1
61
- diverse glomerular histology w/ or w/o MPGN pattern | - C3 alone
C3 glomerulopathy (previously MPGN type 2)
62
types of C3 glomerulopathy
- C3 GN (MPGN type 1 pattern) - DDD - C3 GN (MPGN type 3 pattern)
63
- LM; mesangial proliferation with mesangial interposition and GBM duplication, usually with MEMBRANOUS features - IF; C3 with IgG and/or IgM, C1
MPGN type 3
64
classical complement pathway triggered by what conditions?
- infection - cancer - autoimmune disease - allergic reaction
65
alternative complement pathway HYPERACTIVITY triggered by
- mutations - auto-Abs - monoclonal gammopathy
66
possible treatment for C3 glomerulopathy that targets C5
eculizumab
67
name the 4 possible HCV related GNs
- 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
how many types of cryoglobulins are there?
3
69
cryoglobulinemia - type 1 - what IGs and type?
MONOclonal IgG, IgM, or IgA
70
cryoglobulinemia - type 1 - a/w what diseases?
lymphoproliferative d/o's; MM, WM, CLL, B-cell NHL
71
cryoglobulinemia - type 2 - what IGs and type?
- MONOclonal IgM, IgM, or IgA with RF activity OR - POLYclonal IgG
72
cryoglobulinemia - type 2 - a/w what diseases?
- infections, mainly HCV - autoimmune d/o's - lymphoproliferative d/o's - rarely idiopathic
73
cryoglobulinemia - type 3 - what IGs and type?
POLYclonal mixed IGs (all isotypes) with RF activity from one polyclonal component (usually IgM)
74
cryoglobulinemia - type 3 - a/w what diseases?
- infections, mainly HCV - autoimmune d/o's - rarely idiopathic
75
RF is only positive in which types of cryoglobulinemia?
types 2 and 3
76
hallmark LM and EM findings of cryoglobulinemia
- LM = MPGN, nodular pattern | - EM = precipitating cryoglobulins in glomerulus
77
hallmark laboratory features of HCV-cryoglobulinemic GN
- variable proteinuria - hematuria - renal insufficiency - LOW C4, sometimes low C3 - RF positive (if type 2 or 3) - elevated transaminases in 70%
78
treatment of HCV-associated cryoglobulinemic MPGN - IF mild to moderate proteinuria - IF slow but progressive loss of kidney function - IF eGFR > 50
interferon + ribavirin +/- protease inhibitor
79
treatment of HCV-associated cryoglobulinemic MPGN - IF mild to moderate proteinuria - IF slow but progressive loss of kidney function - IF eGFR < 50
interferon ONLY
80
treatment of HCV-associated cryoglobulinemic MPGN - IF nephrotic range proteinuria - IF rapidly progressive loss of kidney function
- 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
definition of hemolytic-uremic syndrome
- microangiopathic hemolytic anemia (MAHA) - thrombocytopenia - AKI
82
expected laboratory findings of microangiopathic hemolytic anemia (MAHA)
- schistocytes on PBS - elevated LDH - low haptoglobin - elevated bilirubin
83
90% of HUS is typical, which means what?
- caused by Shiga-like toxin | - prodromal episode of diarrhea
84
10% of HUS is "atypical," which means what?
- heterogeneous d/o - NO diarrhea - NO Shiga toxin-producing E. coli infection
85
classification of atypical HUS
``` # familial # sporadic: - idiopathic - pregnancy-associated - HELLP syndrome - drug-induced - organ transplantation - HIV # cancer ```
86
most common protein affected by genetic abnormalities in patients with aHUS
factor H
87
treatment for aHUS
plasmapheresis then eculizumab
88
eculizumab works by targeting
C5
89
Alport syndrome defect in
type 4 collagen α-5 chain gene (COL4A5)
90
most common GN inherited by X-linked pattern
Alport syndrome
91
can Alport syndrome be inherited by AR or AD pattern?
yes
92
clinical presentation of Alport syndrome
- microscopic hematuria - subnephrotic range proteinuria - declining renal function - sensorineural hearing loss - anterior lenticonus of eye
93
diagnosis of Alport syndrome if NO ESTABLISHED family history
renal biopsy
94
renal biopsy findings of Alport syndrome
EM required*** - GBM THICKENING - lamellation --> "BASKET-WEAVE" appearance
95
diagnosis of Alport syndrome if POSITIVE family history
GENETIC TESTING for α3, α4, and α5 chains of type 4 collagen
96
epidemiology of Alport syndrome
MALE predominance
97
thin basement membrane nephropathy renal biopsy findings
``` # EM required*** - diffuse GBM ATTENUATION (thinning) ```
98
epidemiology of thin basement membrane nephropathy
- familial (often), or sporadic | - no gender difference
99
thin basement membrane nephropathy presentation
- microscopic hematuria | - NORMAL renal function
100
thin basement membrane nephropathy AKA
benign familial hematuria
101
thin basement membrane nephropathy caused by
COL4A3 or COL4A4 gene mutation
102
GNs a/w subENDOthelial deposits
- MPGN type 1 - MPGN type 3 - cryoglobulinemia - LN class 3 - LN class 4
103
GNs a/w double contours (same list as GNs a/w subENDOthelial deposits + 2 more)
- MPGN type 1 - MPGN type 3 - cryoglobulinemia - LN class 3 - LN class 4 - TMA - chronic transplant glomerulopathy
104
diffuse thinning of GBM
thin basement membrane disease
105
irregularity and multilayering or splitting of the GBM
Alport’s syndrome
106
diffuse thickening of the GBM
- diabetic nephropathy - hypertensive nephrosclerosis - Alport's disease
107
mainly IgG LINEAR deposition in capillary walls
anti-GBM disease
108
nonspecific LINEAR IgG or "PSEUDOLINEAR" IgG deposition in capillary walls
diabetic nephropathy
109
GRANULAR parietal deposition of IGs and COMPLEMENT | - ***subENDOthelial***
MPGN type 1
110
GRANULAR parietal deposition of IGs and COMPLEMENT | - ***subEPIthelial***
PIGN
111
GRANULAR parietal deposition of IGs and COMPLEMENT | - ***subENDOthelial AND intramembranous***
membranous GN
112
what Ab in granulomatosis with polyangiitis ANCA?
anti-PR3 ANCA
113
what Ab eosinophilic granulomatosis with polyangiitis ANCA?
anti-MPO ANCA
114
ONLY GN with granular pattern on IF AND NORMAL complements
IgA nephropathy
115
GRANULAR parietal deposition of IGs and COMPLEMENT | - ***subENDOthelial, subEPIthelial, AND intramembranous***
MPGN type 3
116
"SAUSAGE-LIKE" (ribbon-like), osmiophilic deposits | - GBM deposits
DDD
117
GN a/w Drusen bodies in retina
DDD (C3 deposition in retina)
118
- MPGN pattern LM - negative IF - ***GBM deposits with ribbon-like pattern***
DDD
119
treatment for DDD
eculizumab
120
- MPGN pattern LM - negative IF - ***subENDOthelial AND mesangial deposits***
C3 GN
121
treatment for C3 GN
rituximab and plasmapheresis

Nephrology Board Review Pearls (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions