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Renal > Robbins - 517-533 - Glomerulus, Nephrotic, Nephritic > Flashcards

Robbins - 517-533 - Glomerulus, Nephrotic, Nephritic Flashcards

1
Q

Glomerular diseases are often ___ mediated

A

Immunologically

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2
Q

___ injury may account for instances of GN in which either there are no deposits of Ab’s or immune complexes

A

T Cell-Mediated injury

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3
Q

___ mechanisms underlie most types of primary glomerular diseases

A

Immune

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4
Q

___ molecules from adjancent foot processes bind to each other thru disulfide bridges

A

Nephrin

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5
Q

2 etiologies of Dense Deposit Disease

A

Auto-Ab to C3 Nephritic Factor - uncontrolled cleavage of C3; Mutations or Auto-Ab’s to Factor H

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6
Q

2 most prevalent primary glomerular diseases in Adults

A
  1. Focal Segmental Glomerulosclerosis; 2. Membranous Nephropathy
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7
Q

2 Typical Features of Immune Complex Disease

A

(1) Hypercomplementemia; (2) Granular deposits of IgG, complement on GBM

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8
Q

3 damaging substances released by Neutrophils

A

Proteases, ROS, AA metabolites

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9
Q

3 most frequent systemic causes of nephrOtic syn in adults are

A

Diabetes, Amyloidosis, SLE

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10
Q

5 manifestations of Nephritic Syndrome

A

Hyper GrAPE: HTN, Gross Hematuria, Azotemia, Proteinuria, Edema

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11
Q

85% of Membranous Nephropathy is caused by

A

Ab’s that cross-react with podocyte antigens

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12
Q

AA metabolites released by Neutrophils cause

A

reduction in GFR

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13
Q

Ab-mediated GN in humans results from

A

Formation of auto-Ab’s directed against GBM

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14
Q

Ab’s against what are suspected when immune complexes are not found in GN

A

Against Glomerular cell antigens

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15
Q

Acute Postinfectious GN is caused by

A

Glomerular deposition of immune complexes; Results in proliferation and damage to glomerular cells and infiltration of leukocytes

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16
Q

After “maladaptive” changes following significant Nephron loss, what happens?

A

Capillary obliteration, Increased deposition of mesangial matrix and plasma proteins, and ultimately sclerosis of glomeruli –> Further reductions in nephron mass

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17
Q

After significant nephron loss, remaining glomeruli tend to undergo ___? This is associated with what hemodynamic changes?

A

Hypertrophy to maintain overall renal fxn; Increases single-nephron GFR, BF, and transcapillary pressure

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18
Q

Age range for IgA Nephropathy

A

Children and Young Adults

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19
Q

Age range for Minimal Change Disease

A

1-7 years

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20
Q

Age range of Membranous Nephropathy

A

30-60, slowly progressive

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21
Q

Alport Syndrome is a mutation in

A

Alpha chains of Type IV Collagen

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22
Q

Alport Syndrome is a type of

A

Hereditary Nephritis

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23
Q

Alport Syndrome is characterized by

A

Nephritis, Nerve Deafness, Eye disorders

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24
Q

Anti-GBM Ab GN is characterized by what IF pattern

A

Linear

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25
Q

Anti-GBM Ab-mediated Crescentic GN is characterized by

A

Linear deposits of Ig, and often C3 on GBM

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26
Q

Anti-GBM Crescentic: Clinical presentation

A

Severe glomerular damage with necrosis and crescents - Rapidly progressive GN

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27
Q

Antibodies directed to what glomerular region tend NOT to elicit inflammation

A

Subepithelial

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28
Q

Antigen in most cases of Membranoproliferative GN

A

Unknown

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29
Q

Antigens in Classic Crescentic GN

A

Fixed antigens in GBM

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30
Q

Auto-Ab to C3 Nephritic Factor - uncontrolled cleavage of C3; Mutations or Auto-Ab’s to Factor H

A

2 etiologies of Dense Deposit Disease

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31
Q

Azotemia, Hematuria, HTN in NephrOtic syn

A

Little to no Azotemia, Hematuria, HTN

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32
Q

Basketweave =

A

Hereditary Nephritis

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33
Q

Best-characterized Anti-GBM GN

A

Classical Anti-GBM Crescentic GN

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34
Q

Causes of MPGN vs DDD

A

MPGN is immune complex deposition vs DDD is Complement dysregulation

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35
Q

Characteristic histological findings in RPGN

A

Crescents

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36
Q

Characteristic IF picture of IgA Nephropathy

A

Mesangial deposition of IgA (often with C3, properdin, and small amounts of IgG or IgM)

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37
Q

Chronic renal disease damages what components of nephron

A

All 4

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38
Q

Classic presentation of Acute Post-Strep GN

A

Nephritic Syndrome

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39
Q

Collapse of Glomerular Tuft and Podocyte Hyperplasia

A

Collapsing Gnephropathy is characterized by

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40
Q

Collapsing Gnephropathy is a variant of

A

FSGS

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41
Q

Collapsing Gnephropathy is characterized by

A

Collapse of Glomerular Tuft and Podocyte Hyperplasia

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42
Q

Complexes deposited in what location tend to elicit inflammatory reaction

A

Endothelium or subendothelium

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43
Q

Crescents can be a complication of any

A

immune complex nephritides

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44
Q

Cut-offs for Proteinuria and Hypoalbuminea in NephrOtic syndrome

A

3.5g proteinuria, 3 g/dL Albumin

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45
Q

DDD (as opposed to Type 1 MPGN) is characterized by

A

Ribbon-like intramembranous deposits

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46
Q

Deposition of Auto-Ab’s directed against GBM show what pattern on IF

A

Linear pattern

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47
Q

Deposition of circulating immune compelxes gives what IF pattern

A

Granular

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48
Q

Diameter of Fenestra

A

70-100 nm

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49
Q

Diameter of Filtration Slits

A

20-30 nm

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50
Q

Early and Late EM changes in Hereditary nephritis

A

Early: Thin GBM; Late: Basketweave

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51
Q

Elevation of BUN and Creatinine; Usually reflects decreased GFR

A

Azotemia

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52
Q

EM findings in Post-infectious GN

A

Subepithelial Humps

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53
Q

Evidence suggests that IgA Nephropathy is an abnormality in

A

IgA production and clearance; Ab’s against abnormally glycated IgA

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54
Q

FSGS is associated with what other conditions

A

HIV, Heroin abuse; Secondary event in other forms of GN

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55
Q

Fundamental Abnormality in Dense Deposit Disease

A

Excessive complement activation

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56
Q

Glomerular lesions from immune complex disease usually consist of

A

Leukocyte infiltration into glomeruli; Variable proliferation of endothelial, mesangial, and parietal epithelial cells

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57
Q

Gross Hematuria, Proteinuira, Azotemia, Edema, HTN: Hyper GrAPE

A

Nephritic Syndrome

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58
Q

Hallmark of IgA Nephropathy

A

Deposition of IgA in Mesangium

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59
Q

Hemodynamic changes caused by Hypertrophy of remaining nephrons in end-stage kidney disease lead to

A

Further endothelial and podocyte injury, increased glomerular permeability to proteins, accumulation of proteins and lipids in mesangial matrix

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60
Q

Hereditary Nephritis is caused by

A

Mutations in genes encoding GBM proteins

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61
Q

Histologic features of glomeruli in FSGS

A

Increased MM, Obliterated capillary lumina, Deposition of hyaline masses and lipid droplets

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62
Q

Histological features shared by Type 1 MPGN and DDD

A

Lobular G, Proliferation of Mesangial and Endothelial cells, Thickened GBM, Tram Track

63
Q

How do immune complexes mainly produce injury in Glomerulus

A

Activation of complement and recruitment of leukocytes

64
Q

How does Membranous Nephropathy contrast to Minimal Change disease

A

No selectivity of proteins, No response to corticosteroids

65
Q

How does Thromin contribute to GN

A

Causes leukocyte infiltration and Glomular Cell proliferation by triggering PAR’s (protease-activated receptors)

66
Q

IF findings in Post-infectious GN

A

Granular deposits of IgG and Complement

67
Q

IF showing deposition principally in mesangial regions

A

IgA Nephropathy

68
Q

IgA Nephropathy is often considered a local variant of

A

Henoch-Schonlein Purpura

69
Q

Inheritance of Hereditary Nephritis

A

Most commonly X-linked

70
Q

Interestitial diseases are more likely caused by

A

Toxic or infectious agents

71
Q

Irregular foci of thickening or attenuation with pronounced splitting and lamination of lamina densa

A

What is basketweave appearance

72
Q

Kidney sin Anti-GBM Ab-mediated Crescentic GN

A

Enlarged and pale with Petechiae

73
Q

LM of Glomeruli in Hereditary Nephritis

A

Normal until late in disease course

74
Q

Lobular G, Proliferation of Mesangial and Endothelial cells, Thickened/Split GBM (tram track)

A

Histological features shared by Type 1 MPGN and DDD

75
Q

Main histologic feature of Membranous Nephropathy

A

Diffuse thickening of capillary wall

76
Q

Manifestation of Hereditary Nephritis

A

Hematuria and slowly progressing proteinuria and declining renal function

77
Q

Manifestation of Minimal Change Disease

A

Insidious nephrotic syndrome in otherwise healthy child

78
Q

Manifestation of Rapidly Progressive GN

A

ProMD: Proteinuria, Microscopic Hematuria, Dysmorphic RBCS, Casts

79
Q

Manifestations of Nephrotic besides Proteinuria, Hypoalbumin, Edema

A

Hyperlipidemia, Lipiduria

80
Q

Membranous Nephropathy is a form of

A

Chronic Immune Complex Glomerulonephritis

81
Q

Membranous Nephropathy is characterized by

A

Subepithelial Ig deposits along GBM

82
Q

Most cases of RPGN are ___ mediated

83
Q

Most characteristic LM change in Post-infectous GN is

A

Increased cellularity of tufts in nearly all glomeruli

84
Q

Most common cause of Nephritic Syndrome worldwide

A

IgA Nephropathy

85
Q

Most common glomerular disease revealed by renal bx worldwide

A

IgA Nephropathy

86
Q

Most important of the primary glomerular lesions that characteristically lead to nephrotic syndrome

A

Focal and Segmental Glomerulosclerosis (Adults); Minimal Change Disease (Children)

87
Q

Most planted antigens induce what pattern in IF microscopy

A

Granular pattern

88
Q

Nephritic syndrome lesions are characterized by

A

Proliferative changes and Leukocyte infiltration

89
Q

Nephrolithiasis is manifested by

A

Renal colic, hematuria, Recurrent stones

90
Q

Normal appearance by LM, but diffuse effacement of foot process by EM

A

Minimal Change Disease

91
Q

Oliguria or Anuria + Recent Onset Azotemia

A

Acute Kidney Injury

92
Q

Once in end-stage renal disease, kidneys show widespread

A

Glomerusclerosis

93
Q

Only visible glomerular abnormality in Minimal Change Disease

A

Uniform and difuse effacement of foot processes of podocytes

94
Q

Onset of IgA Nephropathy

A

Episode of gross hematuria that occurs within 1-2 days of nonspecific URI

95
Q

Onset of Post-infectious GN

96
Q

Pattern of deposits on IF in Membranous Nephropathy

97
Q

Podocytes in EM of FSGS

A

Effacement of Foot Processes

98
Q

Postrenal Azotemia

A

When urine flow is obstructed below level of kidney

99
Q

Prerenal Azotemia

A

Hypoperfusion of Kidneys; Decreases GFR in absence of parenchymal damage

100
Q

Presentation/Age of Hereditary Nephritis

A

Hematuria/Proteinuria at 5-20 years; Renal failure at 20-50 years

101
Q

Primary FSGS accounts for what percent of nephrOtic syn

102
Q

Probably cause of HTN in Nephritic syn

A

Fluid Retention and Increased Renin

103
Q

Prognosis of Acute Post-Infectious GN in children vs adults

A

Most children recover; worse in adults

104
Q

Prognosis of DDD

A

Poor, worse than Type 1 MPGN

105
Q

Prognosis of FSGS

A

Poor, 50% develop end-stage kidney disease in 10 years

106
Q

Prognosis of Minimal Change Disease

A

Good, more than 90% of children respond to short course corticosteroids

107
Q

Prognosis of Type 1 MPGN

108
Q

Progression of FSGS leads to what histological picture

A

Global Sclerosis, Pronounced Tubular Atrophy, Interstitial Fibrosis

109
Q

Proteinuria, Microscopic Hematuria, Dysmorphic RBCS, Casts

A

Manifestation of Rapidly Progressive GN

110
Q

Puzzling aspect of Membranous Nephropathy

A

Immune complexes cause capillary damage in absence of inflammatory cells (likely via complement instead)

111
Q

RAAS in Nephrotic Syndrome

A

Activated due to decreased intravascular volume

112
Q

Renal colic, hematuria, Recurrent stones

A

Nephrolithiasis is manifested by

113
Q

Renal function in Minimal Change Disease

A

preserved in most children

114
Q

RPGN is characterized by

A

Progressive loss of renal function, Lab findings of Nephritic Syndrome, often severe oliguria

115
Q

Segmental distribution of necrotizing and crescentic GN is typical of

A

ANCA-associated crescentic GN

116
Q

Spike and Dome =

A

Membranous Nephropathy

117
Q

Subepithelial Humps =

A

Post-infectious GN

118
Q

The classic case of poststrep GN develops in

A

a child 1-4 weeks after GAS infection

119
Q

The major component of slit diaphragms

120
Q

Timeline of Rapidly Progressive Glomerulonephritis

A

Fews days or weeks

121
Q

Tissue injury in Post-Strep GN is primarily caused by

A

complement activation by the classical pathway

122
Q

Tram Track =

123
Q

Tubular diseases are more likely caused by

A

Toxic or infectious agents

124
Q

Two possible causes of Membranoproliferative GN

A

Circulating immune complexes, or planted antigen the in situ complex formation

125
Q

Tx of Anti-GBM Ab-mediated Crescentic GN

A

Plasmapharesis

126
Q

Tx of Minimal Change Disease

A

Corticosteroids

127
Q

Type 1 MPGN (as opposed to DDD) is characterized by

A

Discrete subendothelial electron-dense deposits

128
Q

Type of Collagen in GBM

129
Q

Types of “planted” antigens

A

Nucleosomal complexes, Bacterial products, Large aggregated proteins, Immune complexes

130
Q

Uremia

A

When Azotemia gives rise to clinical manifestations and systemic biochemical abnormalities

131
Q

Urine in Post-Infectious GN

A

Gross Hematuria (smoky brown), Some proteinuria

132
Q

Visceral Epithelial Cells =

133
Q

Well-develped Membranous Nephrophy shows

A

Diffuse thickening of capillary wall

134
Q

What can reverse podocyte changes in Minimal Change Disease

A

Corticosteroids

135
Q

What causes 65% of primary glomerual disease in children?

A

Minimal Change Disease

136
Q

What causes the “splitting of the GBM” (tram track)?

A

Extension of processes of mesangial and inflammatory cells into peripheral capillary loops and deposition of mesangial matrix

137
Q

What conformational change appears to be key to auto-Ab attack of GBM

A

Alpha3 subtupe of Type IV collagen

138
Q

What does Azotemia usually reflect

A

Decreased GFR

139
Q

What endogenous podocyte antigen is most recognized by causative Auto-Ab’s in Membranous Nephropathy?

A

PLA2 receptor

140
Q

What forms crescents in RPGN

A

Proliferation of Parietal Cells and Migration of Monocytes/Macrophages in Bowman’s space

141
Q

What is Azotemia?

A

Elevation of BUN and Creatinine; Usually reflects decreased GFR

142
Q

What is basketweave appearance

A

Irregular foci of thickening or attenuation with pronounced splitting and lamination of lamina densa

143
Q

What is more pronounced in RPGN than in Nephritic Syndrome

A

Oliguria and Azotemia

144
Q

What is the Tram Track

A

Thickened GBM with double contour glomerular capillary wall in MPGN

145
Q

What is thought to cause injury in neutrophil-independent GN

A

Complement, MAC

146
Q

What is thought to represent initiating event in FSGS?

A

Injury to podocytes

147
Q

What likely damages mesangial cells and podocytes in Membranous Nephropathy

A

MAC activated by Immune Complexes

148
Q

What mutation seems to be strongly associated with increased risk of FSGS and renal fialure in AA’s

149
Q

What percent of GFR is reduced before inexorable progression to end-stage kidney disease

150
Q

What predicts progression and response to intervention in IgA Nephropathy?

151
Q

When anti-GBM Ab’s cross react with BM of lungs

A

Goodpasture Syndrome

152
Q

When Azotemia gives rise to clinical manifestations and systemic biochemical abnormalities

153
Q

Which are permeable in glomerulus: cations or anions?

A

Cations - More cationic, more permeable

154
Q

Which RPGN subtype shows segmental necrosis?

Renal (31 decks)

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