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Renal SOH > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

Definition

A

Immune mediated disease which affects the glomeruli.

Disruption of the glomerular capillary wall

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2
Q

Which 3 parts of the glomerulus can be affected?

A

Endothelium
Basement membrane
Podocytes

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3
Q

Causes

A 
Idiopathic
Infections
Drugs 
Malignancies 
Small vessel vasculitis 
Lupus 
Goodpastures
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4
Q

Pathology

A

Depends on site of injury

Depends on type of injury

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5
Q

Proliferative or non proliferative refers to…

A

Presence or absence of proliferation of mesangial cells

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6
Q

Focal or diffuse refers to…

A

How much of the glomeruli are affected

  • focal = less than 50% affected
  • diffuse = more than 50% affected
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7
Q

Global or segmental refers to…

A

Global - all glomerulus affected

Segmental - parts of glomerulus affected

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8
Q

Cresenteric refers to…

A

Presence of a crescent of cells

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9
Q

Crescents is a manifestation of mild/severe glomerular damage

A

Severe

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10
Q

Damage to mesangial cells leads to proliferative/non-proliferative lesion

A

Proliferative

- mesangial cells proliferate and release angiotensin II

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11
Q

Damage to mesangial cells - urine

A

Leakage occurs through the glomerular wall resulting in

  • haematuria
  • proteinuria
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12
Q

Damage to mesangial cells - inflammatory or non inflammatory process?

A

Inflammatory

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13
Q

Can damage to mesangial cells result in renal failure?

A

Yes

- gradual progression of renal failure

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14
Q

Damage to endothelial cells - proliferative or non-proliferative lesion?

A

Proliferative

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15
Q

Damage to endothelial cells - inflammatory or non inflammatory process?

A

Inflammatory

- inflammation of the endothelium

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16
Q

Which condition does damage to the endothelial cells result in?

A

Vasculitis

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17
Q

Damage to endothelial cells - urine

A

Leakage occurs through the glomerular wall resulting in

- haematuria

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18
Q

Can damage to endothelial cells result in renal failure?

A

Yes

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19
Q

Damage to endothelial cells results in a very rapid decline in the patient. True or false?

A

True

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20
Q

Damage to podocytes leads to a proliferative or non proliferative lesion?

A

Non-proliferative

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21
Q

Damage to podocytes involves an inflammatory or non-inflammatory process?

A

Non-inflammatory process

- podocytes shrink back and they are no longer an effective barrier

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22
Q

Damage to podocytes - urine

A

Leakage occurs through the exposed glomerular wall resulting in

  • haematuria
  • proteinuria
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23
Q

What is the range of microalbuminuria

A

30-300mg albuminuria/day

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24
Q

Asymptomatic proteinuria range

A

<1g/day

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25
Q

Heavy proteinuria range

A

1-3g/day

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26
Q

Nephrotic range of proteinuria

A

> 3g/day

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27
Q

Glomerulonephritis causes a decreased production of urine. True or false?

A

True

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28
Q

AKI due to glomerulonephritis is most commonly due to

  • damage to mesangial cells
  • damage to endothelial cells
  • damage to podocytes
A

Damage to endothelial cells

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29
Q

Investigations

A 
Blood tests 
Urinalysis 
Urine microscopy
Renal biopsy
Immunofluoresence 
Electron microscopy
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30
Q

Investigations - urine microscopy findings

A

Dysmorphic RBCs
- since they are squeezed through damaged glomerulus

RBC and granular casts
- small tubule shaped prticles which get washed into the urine

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31
Q

What do the presence of granular casts suggest?

A

There is an active inflammatory process

  • damage to mesangial cells
  • damage to endothelial cells
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32
Q

If urinalysis reveals proteinuria, what is the next investigation to do?

A

24 hour urine collection to quantify the proteinuria

33
Q

Investigations - What is the purpose of immunofluoresence?

A

Look for circulating immune complexes

34
Q

Investigations - what is the purpose of electron microscopy?

A

Shows how cells are affected

35
Q

Proteinuria impacts on how quickly the disease progresses - true or false?

A

True

36
Q

Management - aims

A

Reduce degree of proteinuria

Preserve long term renal function

37
Q

Target BP in a patient with proteinuria?

A

Less than 130/80

38
Q

Management - medications

A 
ACE inhibitors 
ARBs 
Diuretics 
Statins 
Anticoagulants/antiplatelets
39
Q

Management - immunosuppressive therapy

A

Corticosteroids
Azathioprine
Cyclophosphamides

40
Q

Is plasmaphoresis of use in GN?

A

Yes

- rapidly removes the antibody whilst the drugs start to work

41
Q

Rapidly progressive glomerulonephritis (RPGN) is a treatable cause of AKI. True or false?

A

True

42
Q

What is likely to be seen on renal biopsy of RPGN patient?

A

Granular casts

43
Q

Management of RPGN

A 
Treat ASAP
Strong steroids 
Cyclophosphamide 
Plasmapheresis 
Supportive care
44
Q

Nephrotic syndrome

A

Disorder of glomerular filtration allowing protein to appear in filtrate, resulting in proteinuria

45
Q

Nephrotic syndrome - clinical features

A

Oedema (everywhere)
Proteinuria
HypoalbuminAEMIA
HypercholesterolAEMIA

46
Q

Why does oedema occur in nephrotic syndrome

A

Patients are loosing protein faster than they can make it

Fluid leaks out into the interstitium

47
Q

Renal function is usually normal in nephrotic syndrome. True or false?

A

True

- normal creatinine level

48
Q

Nephrotic syndrome is most likely due to a proliferative or non-proliferative process?

A

Non proliferative

- affecting the podocytes

49
Q

Nephrotic syndrome - management

A 
Fluid restriction
Salt restriction
Diuretics
ACE inhibitor or ARBs
Anticoagulation
50
Q

Patients with nephrotic syndrome are more or less susceptible to infection?

A

More

- peeing out proteins (Ig)

51
Q

Nephritic syndrome is most likely due to a proliferative or non-proliferative process?

A

Proliferative

  • damage to the mesangial cells
  • damage to the endothelial cells
52
Q

Nephritic syndrome - clinical features

A 
AKI 
Oliguria
Oedema
Haematuria 
Hypertension
53
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change nephropathy

54
Q

Minimal change nephropathy is due to damage of… ?

  • mesangial cells
  • endothelial cells
  • podocytes
A

Podocytes

55
Q

Who gets minimal change nephropathy?

A

Children

56
Q

Minimal change nephropathy - Renal biopsy appearance?

A

Looks normal

57
Q

Electron microcopy is a good way to visualise podocytes?

A

True

58
Q

Minimal change nephropathy - management

A

Oral steroids

Cyclophosphamide

59
Q

Focal segmental glomerulosclerosis nephropathy (FSGS) is due to damage of ?

  • mesangial cells
  • endothelial cells
  • podocytes
A

Podocytes

60
Q

FSGS is more common in adults or children?

A

Adults

61
Q

What is the most common cause of nephrotic syndrome in adults?

A

FSGS

62
Q

FSGS - pathology

A

Patches of focal sclerosis

63
Q

FSGS - causes

A

HIV
Heroin use
Obesity
Reflux nephropathy

64
Q

FSGS renal biopsy appearance

A

Focal segmental glomerulosclerosis

  • only some glomeruli are affected
  • only some parts are affected
65
Q

FSGS - management

A

Prolonged steroids

66
Q

What is the most common cause of nephrotic syndrome in the UK?

A

Membranous nephropathy

67
Q

Membranous nephropathy - definition

A

Thickening of the glomerular BM

68
Q

Membranous nephropathy - causes

A

Infections
CTD (lupus)
Malignancy

69
Q

Membranous nephropathy - immunology

A

IgG attaaches to podocytes and causes podocyte damage

70
Q

Membranous nephropathy renal biopsy appearance

A

Thickening of the glomerular BM (silver stain)

Immune complex deposition between podocytes

71
Q

Membranous nephropathy - management

A

Steroids
Immunosuppression (if steroids don’t work)
MABs

72
Q

Patients with membranous nephropathy can progress to ESRF?

A

True

73
Q

What is the commonest GN in the world?

A

IgA nephropathy

74
Q

IgA nephropathy - immunopathogenesis

A

Wonky IgA

75
Q

IgA nephropathy - cause

A

Infection

- More IgA production and therefore more kidney inflammation

76
Q

Patient develops macroscopic haematuria after a resp infection. What is the most likely diagnosis?

A

IgA nephropathy

77
Q

IgA nephropathy - associated condition

A

HSP (small vessel vasculitis)

78
Q

IgA nephropathy - renal biopsy appearance

A

Mesangial cell proliferation and expansion

79
Q

IgA nephropathy - management

A

BP control

Renal SOH (25 decks)

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