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Renal and Urology > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

definition

A

any immune mediated disease of the kidneys which affects the glomerulus (which causes secondary tubule-interstitial disease)

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2
Q

Damage to the endothelial or mesangial cells causes a what type of lesion?

A

proliferative lesion and causes red blood cells in the urine

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3
Q

damage to the podocytes causes a what type of lesion?

A

non-proliferative lesion with protein in the urine

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4
Q

why does damage to the podocytes cause a non-proliferative lesion

A

because damage to the podocytes causes atrophy

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5
Q

damage to the endothelial cells causes a

A

vasculitis

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6
Q

damage to the mesangial cells causes

A

the attraction of inflammatory cells

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7
Q

key investigations for any person presenting with suspected glomerulonephritis

A
  • urinalysis= shows proteinuria or red blood cells
  • urine microscopy= may show dysmorphic red block cells, lipiduria, red blood cells or glomerular casts
  • 24 hour urine protein must be carried out as this is required to diagnose nephrotic syndrome
  • FBCS= platelets and creatinine
  • renal biopsy is the conclusive investigation
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8
Q

haematuria is either

A

asymptomatic microscopic haematuria or painless macroscopic haematuria

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9
Q

proteinuria quantification

A
  • microalbuminuria (30-300mg albumin/day)
  • asymptomatic protineuria (less than 1g/day)
  • heavy proteinuria (1-3g per day)
  • nephrotic range of proteinuria (more than 3g per day)
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10
Q

nephrotic syndrome

A
  • proteinuria greater than 3g per day
  • hypoalbunaemia (less than 30)
  • hypercholesterolaemia
  • oedema
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11
Q

nephrotic syndrome is indicative of a process affecting what type of cell

A

Podocytes

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12
Q

in nephrotic syndrome the loss of protein in the urine causes

A

hypoalbunaemia which causes a fall in the capillary oncotic pressure which causes fluid to shift from the vasculature into the tissues (albumin is the major protein which keeps fluid in the vasculature)

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13
Q

because of the hypoalabunaemia the liver

A

starts increasing its production of albumin but also increases its production of cholesterol which is not required causing hypercholesterolaemia

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14
Q

the proteins lost in neprhtoci syndrome also includes the loss of

A

antibodies (which are essentially proteins) so person is at increased risk of infection

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15
Q

reduced volume within the vasculature means

A

there is reduced venous return to the heart which causes reduced cardiac output which causes renal hypo perfusion which increased the risk of an AKI and causes the juxtaglomerular cells to produce renin which activates the RAAS system

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16
Q

what else is lost in nephrotic syndrome

A

anti-thrombin 3 which increases the risk of renal vein thrombi and pulmonary emboli

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17
Q

signs and symptoms of nephrotic syndrome

A
  • xathelasma and xanthomata caused by hypercholesterolaemia

- leukonychia, peri-orbital oedema and peripheral oedema caused by hypoalbuminaemia

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18
Q

in nephrotic syndrome urine is described as

A

frothy in appearance

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19
Q

nephritic syndorme is indicative of

A

a proliferative process affecting endothelial cells

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20
Q

pathophysiology of nephritic syndrome

A

immune complexes get lodged in the glomerulus and elicit an inflammatory response with the recruitment of white cell causing damage allowing red blood cell to pass through into the filtrate

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21
Q

components of nephritic syndrome

A
  • haematuria
  • oliguria because the glomerulus is being damaged there is a reduction in glomerular filtration rate
  • hypertension
  • proteinuria can also occur but not to the same extent as in nephrotic syndrome
  • active urinary sedimant= red blood cells, white blood cells and granular casts
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22
Q

classification of glomerulonephritis

A

classified according to its aetiology and histology

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23
Q

aetiology of glomerulonephritis

A

can be primary (idiopathic) which actually accounts for the majority of cases or secondary (caused by infection, drugs, malignancy or an underlying systemic disease)

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24
Q

histology of GN

A
  • renal biopsy is examined under light microscopy, electron microscopy and immunofluorescence
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25
Q

histological classifications

A
  • proliferative or non-proliferative (presence or absence of proliferation of mesangial cells)
  • focal or diffuse (focal involves less than 50% of the glomeruli, diffuse involves more than 50% of the glomeruli)
  • global or segmental (global involves the whole glomerulus, segmental only involves part of the glomerulus)
  • Cresentic (presence of crescents: epithelial extra-capillary proliferation)
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26
Q

minimal change disease causes a

A

nephrotic syndrome

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27
Q

minimal change disease if the most common cause of what

A

nephrotic syndorme in children

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28
Q

pathophysiology of minimal change disease

A

podocytes have for processes which have a negatively charged coat which repels negatively charged molecules such as albumin, in minimal change disease T cells release cytokines which specifically damages the foot processes of the podocytes causing them to flatten out in a process called effacement , the change allows albumin to pass into bowmans capsule but does not allow other larger proteins through so there is a selective proteinuria

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29
Q

foot process effacement in minimal change disease

A

cannot be seen on light microscopy hence the name minimal change disease however, on electron microscopy foot process effacement can be seen

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30
Q

on immunofluorescence for minimal change disease

A

it is negative because the damage is caused by cytokines not immune complex deposition

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31
Q

minimal change disease will not cause

A

progressive renal failure

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32
Q

do you carry out renal biopsies for minimal change disease

A

only if it is unresponsive to steroids

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33
Q

treatment of minimal change disease

A
  • 1st line= very response to oral steroid

- 2nd line= cyclophosphamide

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34
Q

focal segmental glomerulosclerosis causes a

A

Nephrotic syndrome

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35
Q

focal segmental glomerulosclerosis is the most common cause of what

A

nephrotic syndorme in adults

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36
Q

FSGS by breaking the work down

A
  • focal means less than 50% of the glomeruli are affected
  • segmental means only part of the glomeruli are affected
  • glomerulosclerosis means scarring of the glomerulus occurs
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37
Q

FSGS can be

A

primary or secondary

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38
Q

primary FSGS means

A

idiopathic, podocytes are damaged and allow proteins and lipids into the filtrate, over time proteins and lipids get trapped in the glomerulus causing hyalinosis (tissue has a glassy appearance on histology) which eventually causes glomerulosclerosis

39
Q

secondary FSGS

A
  • HIV (HIV associated nephropathy)
  • Heroin (heroin associated nephropathy)
  • Sickle cell disease
40
Q

Histology of focal segmental glomerulosclerosis

A

segmental sclerosis and hyalinosis

41
Q

electron microscopy of FSGS

A

foot process effacement

42
Q

on immunofluoresces of FSGS

A

there may be non-specific focal despots of IgM and comleemtn proteins (but this is not always present)

43
Q

treatment of focal segemtla glomerulosclerosis

A

60% achieve remission with prolonged steroids but 50% progress to end stage renal failure within 10 years

44
Q

membranous nephropahty cuases a

A

nephrotic syndrome

45
Q

membranous nephrotpathy is caused by

A

damage and inflammation to the glomerular basement membrane which causes the basement membrane to become more permeable allowing proteins to enter the filtrate

46
Q

membranous nephropathy is the

A

second most common cause of nephrotic syndrome in adults

47
Q

the damage in membranous nephropathy is caused by

A

immune complexes either autoantibodies directly targeting the glomerular basement membrane or immune complexes formed outside the kidney and deposit in the glomerular basement membrane

48
Q

immune complexes in membranous glomerulonephritis are called

A

sub-epithelial deposits because they are between the podocytes and the glomeruarl basement membrane

49
Q

sub-epithelial deposits activate the

A

complment system which produces membrane attack complex which damages the podocytes and mesangial cells

50
Q

mesnagial cells are the cells

A

that remove debris

51
Q

the immune reaction occurring in membranous nephropathy also

A

recruits inflammatory cells which release proteases and oxidants causing damage to the GBM, over time as a reaction to the immune deposits GBM matrix gets laid down between the immune complexes which makes the GBM appear thicker on histology

52
Q

in membranous nephropathy/ glomerulonephritis on electron microscopy

A

there is a characteristic spike and dome pattern

53
Q

on immunoflourecence for membranous nephropathy there are

A

deposits of immune complex

54
Q

membranous nephropahty is usually

A

primary (idiopathic) there other cases are secondary and are caused by autoantibodies generated in response to infection (hep B), malignancy (lymphoma, carcinomas), auto-immune disease (SLE), drugs (penicillaemine, gold)

55
Q

why is it important to known whether membranous nephrotpathy is primary or secondary

A

because if someone has secondary nephropathy and you treat them as you would in primary it could kill them i.e. someone with hep B

56
Q

treatment of primary membranous nephropathy

A

Steroids/alkyalting agents/ B cell monoclonal antibodies

57
Q

treatment of secondary membanous nephropathy

A

treat the underlying cause

58
Q

30% of people with membranous glomerulonephritis

A

progress to end stage renal failure within 10 years

59
Q

IgA nephropathy is the

A

commonest type of glomerulonephritis in the world

60
Q

IgA nephropathy occurs when an

A

abnormal IgA froms and deposits in the kidneys causing damage

61
Q

in IgA nephropahty the

A

abnormal glycosylation of the hinge region of the IgA1 causing them to be galactose deficienct so they are not recognised by the body and accumulate, they are also considered to be non-self so the body generates IgG antibodies in reponse which bind to abnormal IgA-1 forming an immune complex and deposit at sites throughout the body

62
Q

the abnormal immune complexes specifically deposit in

A

the mesangium which activates the alternative complement pathway leading to the release of pro-inflammatory cytokines and the migration of macrophages causing glomerular injury allowing red blood cells to enter the filtrate causing a nephritic syndrome

63
Q

IgA nephropathy causes a

A

nephritic syndrome

64
Q

IgA nephropathy classically present in

A

childhood as a microscopic or macroscopic haematuria and usually develops during an infection involving the mucosal lining (infection of the GI or respiratory tract)

65
Q

During each infections in IgA nephropathy

A

there is increased production of IgA-1 so there is increased immune complex deposition therefore, over many decades it can progress to end stage renal failure

66
Q

in IgA nephropathy there is what seen on light microscopy

A

meangial cell proliferation

67
Q

in IgA nephropathy there is what seen on electron microscopy

A

IgA immune complex deposition in the measngium (and on immunofluorescence)

68
Q

IgA nephroapthy is associated with

A

hence schoenlen purpura but HSP affects other parts of the body

69
Q

treatment of IgA nephropathy

A
  • once the kdiensy have been scarred this cannot be reversed however progression can be slowed by blood pressure control (reducing salt intake and ACE inhibitors)
70
Q

post-streptococcal glomerulonephritis

A

glomeruli become inflamed after a streptococcal infection (commonly group A strep)

71
Q

infection by group A strep initiates a

A

type 3 hypersensitivity reaction where immune complexes are formed (often IgG or IgM antibodies) which deposit in the glomerular basement membrane at the sub-epithelium, this causes an inflammatory reaction causing activation and deposition of C3 complement and release of inflammatory cytokines and proteases which damage the glomerulus and allows protein and red blood cells into the urien

72
Q

post- streptococcal glomerullonephritis causes a

A

nephritic syndrome

73
Q

post-streptococcal glomerulonephritis usually affects

A

children

  • either 1-2 weeks after a throat infection
  • 6 weeks after a skin infection such as impetigo
74
Q

on light microscopy for post-streptococcal glomerulonephritis

A

the glomerulus looks enlarged

75
Q

on electron microscopy for post-streptococcal glomerulonephritis there is

A

sub-epithelial depostiion

76
Q

on immunofluorescence for post-streptococcal GN

A

there is a starry sky granular appearance of the GBM and mesangium

77
Q

blood test in post-strep GN show

A
  • antibodies against group A strep

- decreased complement levels

78
Q

treatment for post-streptococcal glomerulonephritis

A

usually is spontaneously resolving but in some children can develop acute renal failure and one quarter of adults with post-streptococall GN develop rapidly progressive GN

79
Q

rapidly progressive glomerulonephritis is also called

A

crescentic glomerulonephritis

80
Q

rapidly progressive glomerulonephritis causes a type of

A

nephritic syndrome

81
Q

inflammation of the glomerulus causes

A

proliferation of the cells in bowmans space forming a crescent shape which leads to renal failure within days/ weeks

82
Q

rapidly progressive glomerulonephritis can be

A

idiopathic or if there is a known cause it is categorised

83
Q

type 1 rapidly progressive GN

A

anti-glomerular basement membrane antibodies as seen in good pastures syndrome

84
Q

type 2 rapidly progressive GN

A

immune complex mediated as seen in post-streptococcal GN, SLE, IGA NEPHROPAHY AND HENOCH SCHOENLEN PURPURA

85
Q

Type 3 rapidly progressive GN

A

paucci immune (no anti-GBM and no immune complexes) ANCA is seen (anti- neutrophil cytoplasmic antibodies) which are antibodies against the bodies own neutrophils

86
Q

type 3 is further divided into

A

c-ANCA and p-ANCA

87
Q

c-ANCA is seen in

A

GPA

88
Q

p-ANCA is seen in

A

microscopic polyangittis and eosinohilis grnaulomatosis with polyangiiits

89
Q

typically in rapidly progressive GN because of

A

cell mediated immunity and macrophages involvement the GBM breaks allowing red blood cells, inflammatory mediators, proteins and fibrin to enter the bowmans space, this allows monocytes and macrophages to enter bowmans spaces as well as parental epithelial cells which proliferate forming a thick characteristic crescent shape, over time crescent ca undergo sclerosis and be replaced with connect tissue

90
Q

on light microscopy rapidly progressive GN shows

A

a crescent shape

91
Q

the types of secondary rapidly progressive GN can be differentiated using

A

immunofluorescence
type 1= linear pattern
type 2= granular pattern
type 3= negative as it is pouch immune

92
Q

treatment of rapidly progressive GN shouldd be

A

prompt with potent immunosuppression with supportive dialysis if required

93
Q

immunosuppression used

A

steroids or cytotoxic (cyclophosphamide/ mycopentolate/ azathioprine), plasmapheresis is usually sued in combination

Renal and Urology (51 decks)

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