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Nephrology > Glomerular Structure and Mechanisms of Disease > Flashcards

Glomerular Structure and Mechanisms of Disease Flashcards

1
Q

Name 9 places in a glomerulus that disease can be located.

A
  1. Arterioles 2. Capillaries
  2. Subendothelial 4. GBM
  3. Subepithelial 6. Slit pore diaphragm
  4. Podocytes 8. Bowman space/capsule
  5. Mesangium
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2
Q

Name 8 primary glomerular diseases.

A
  1. Minimal change disease
  2. Focal segmental glomerulosclerosis
  3. Membranous nephropathy
  4. Acute post-streptococcal glomerulonephritis
  5. Membranoproliferative glomerulonephritis
  6. IgA nephropathy (Berger disease)
  7. Hereditary nephritis (Alport syndrome)
  8. Congenital nephrotic syndrome
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3
Q

Name 5 secondary glomerular diseases.

A
  1. Hypertensive nephropathy
  2. Diabetic nephropathy
  3. Lupus nephritis
  4. Amyloidosis
  5. Goodpasture syndrome
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4
Q

Name the three most common types of glomerular disease.

A
  1. Hypertensive
  2. Diabetic
  3. Immune-mediated
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5
Q

What do supra-normal glomerular capillary pressures result in?

A

GBM thickening
Mesangial cell hypertrophy/hyperplasia,
Mesangial matrix production
Hyaline sclerosis of afferent arterioles

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6
Q

What is the term for global sclerosis of glomeruli?

A

Arterionephrosclerosis

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7
Q

Why is arterionephrosclerosis more common in African Americans?

A

Mutation of apolipoprotein L1 (normally confers Trypanosoma resistance)

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8
Q

What two conditions are a mutation in apoL1 associated with?

A

Arterionephrosclerosis

Focal segmental glomerulosclerosis

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9
Q

What are the symptoms/signs of malignant hypertension?

A 
BP > 200/120
Headache
Hematuria / Proteinuria
Scotomas
Vomitting
Onion-skin appearance (proliferation of intimal cells in arteries; hyperplastic arteriosclerosis)
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10
Q

What does malignant hypertension produce?

A

Fibrinoid necrosis of arterioles

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11
Q

What category of disease does injury to glomerular capillary endothelium cause?

A

Thrombotic microangiopathies

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12
Q

What are the layers of the glomerular basement membrane?

A 
Lamina rara (or lucida) interna
Lamina densa (double usual thickness)
Lamina rara externa
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13
Q

What are the major components of the basement membrane?

A 
Type IV collagen
Perlecan
Entactin
Fibronectin
Laminin
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14
Q

What is the composition and function of perlecan?

A

Highly charged proteoglycan w/ heparan sulfate keeps proteins (ie albumin) from being filtered

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15
Q

What is the function of entactin?

A

Glycoprotein with calcium binding properties

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16
Q

What is the function of fibronectin?

A

Glycoprotein binds collagen, heparan sulfate, and integrins

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17
Q

What is the function of laminin?

A

Binds collagen, entactin, heparan sulfate, and cells (integrins)

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18
Q

What heterotrimers are present in adult type IV collagen?

A

alpha3, alpha4, alpha5

alpha5, alpha5, alpha6

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19
Q

What is a cause of glomerulonephritis with hematuria?

A

Antibody against epitope in the NC1 domain of the alpha3 chain

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20
Q

Which gender has a thicker glomerular basement membrane?

A

Men

21
Q

Which gender has a higher incidence of anti-GBM disease?

A

Men

22
Q

What happens to podocytes during nephrotic syndrome?

A

Effacement

23
Q

What causes crescentic glomerulonephritis and what is the pathology?

A

Nephrotic syndrome with inflammatory stimuli lead to proliferation of parietal epithelial cells

24
Q

Name 4 proteins involved in the slit pore diaphragm.

A

Cadherin and FAT - bind adjacent pedicles

Nephrin and podocin - play a role in filtration

25
Q

What is a potential cause of congenital nephrotic syndromes?

A

Mutations in nephrin and podocin

26
Q

What causes IgA nephropathy?

A

Reduced glycosylation in the hinge region of IgA1

27
Q

What can IgA form immune complexes with?

A

IgA
IgG
Fibronectin
CD89 (soluble IgA receptor)

28
Q

What do the immune complexes bind to that triggers phagocytosis?

A

CD71 (transferrin receptor on mesangial cells)

29
Q

What produces the injurious inflammation in IgA nephropathy?

A

Complement activation

75% Alternative - 25% Lectin

30
Q

Define deposited and in situ immune complexes.

A

Deposited - originated in circulation

In situ - formed in glomerulus

31
Q

Define intrinsic and planted antigens.

A

Intrinsic - fixed in glomerulus

Planted - from circulation

32
Q

What mechanisms typically cause damage in immune-mediated glomerular disease?

A

Complement activation and leukocyte mechanisms

33
Q

How do leukocytes cause glomerular injury?

A

Lysosomal proteases
ROS
Arachidonic acid metabolites

34
Q

How do platelets cause glomerular injury?

A

Aggregation

Arachidonic acid metabolites

35
Q

How do endothelial cells cause glomerular injury?

A 
Cytokines (IL-1)
Arachidonic acid metabolites
Growth factors
Nitric oxide
Endothelin
36
Q

How do glomerular epithelial and mesangial cells cause glomerular injury?

A

Cytokines (IL-1)
Arachidonic acid metabolites
Growth factors

37
Q

What is a hallmark histopathology of lupus nephritis?

A

Subendothelial deposits thickening capillary walls that resemble “wire loops.”

38
Q

What location do poststreptococcal glomerulonephritis antigens plant?

A

Subepithelium (characteristic “humps”)

39
Q

What do antibodies against phospholipase A2 receptors of podocytes cause?

A

Membranous glomerulonephritis

40
Q

What are the antibodies in post-streptococcal glomerulonephritis against?

A

Streptococcal exotoxin B
Streptococcal GAPDH
Endostroptosin

41
Q

What three forms of microscopy are needed to diagnose kidney immune complex disease?

A

Light microscopy
Immunofluorescence
Electron microscopy

42
Q

What stains are used in light microscopy when studying immune glomerular disease?

A

H&E
Jones methenamine silver (GBM)
periodic acid Schiff (cytoplasmic inclusions)
trichome (collagen)

43
Q

The largest subset of crescentic glomerulonephritis is described as what?

A

Pauci-immune (typically ANCA+)

44
Q

What are P-ANCA and C-ANCA associated with?

A

P-ANCA - microscopic polyangiitis or Churg-Strauss syndrome

C-ANCA - granulomatous with polyangiitis or Wegener’s

45
Q

What does hyperglycemia cause in the blood and GBM?

A

Glycosylation of proteins
Thickening of GBM
Deposits on GBM

46
Q

What causes the characteristic effect of diabetes mellitus on organs throughout the body?

A

Metabolization of glycosylated proteins to advanced glycation end-products (AGE)

47
Q

What activate/induce NADPH oxidases (producing ROS)?

A

Advanced glycation end-products (AGE)
Advanced oxidation protein products (AOPP)
Renin Angiotensin System (RAS)
TGF-beta

48
Q

What does activated NADPH oxidases (and ROS) cause in the kidney?

A

Mesangial cell hypertrophy / hyperplasia
Mesangial matrix production
Podocyte injury / apoptosis

49
Q

What does hypertension cause in the glomerulus?

A

GBM thickening
Mesangial cell hypertrophy / hyperplasia
Mesangial matrix production

Nephrology (18 decks)

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