Glomerulonephritis Flashcards

1
Q

What?

A

Immune mediated disease of kidneys affecting glomeruli

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2
Q

Types?

A
Idiopathic GN 
Minimal change nephropathy 
FSGS 
Membranous nephropathy 
IgA nephropathy 
RPGN
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3
Q

Pathogenesis?

A

Humoral (antibody mediated)
Cell- mediated (T cells)
Inflammatory cells, mediators and complements

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4
Q

What does damage to endothelial or mesangial cells lead to?

A

Proliferative lesions and red cells in urine

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5
Q

What does damage to podocytes lead to?

A

Non- proliferative lesion and protein in urine

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6
Q

What causes atrophy?

A

Podocyte damage

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7
Q

Microalbuminuria?

A

30- 300mg albuminuria/ day

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8
Q

Asymptomatic proteinuria?

A

<1g/ day

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9
Q

Heavy proteinuria?

A

1-3g/ day

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10
Q

Nephrotic syndrome proteinuria?

A

> 3g proteinuria/ day

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11
Q

Clinical presentations of glomerulonephritis?

A
Haematuria
Proteinuria
Urine microscopy - RBC 
Red cell casts
Impaired renal function
Hypertension
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12
Q

Nephrotic syndrome?

A

Heavy proteinuria
Hypoalbuminaemia
Fluid retention

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13
Q

Nephritic syndrome?

A
Haematuria
Proteinuria
Fall in GFR
Salt and water retention
Hypertension
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14
Q

Rapidly progressive glomeurlonephritis?

A

Rapid loss of renal function

ESRD within weeks/ months

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15
Q

Chronic glomerulonephritis?

A

Much slower deterioration in renal function

Haematuria, proteinuria, hypertension

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16
Q

Investigations?

A
Urine dipstick and microscopy
Urine protein quantification
GFR
FBC, ESR, CRP
Biochemistry
Glucose
Serum immunoglobulins, serum and urine protein electrophoresis 
Serum complement 
Autoantibodies 
HBsAg
Radiology 
RENAL BIOPSY
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17
Q

Urine dipstick and microscopy?

A

Haematuria and/ or proteinuria

Red cell casts

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18
Q

Urine protein quantification?

A

24 hour urine sample or protein: creatinine ratio

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19
Q

Biochemistry?

A
Renal function
Electrolytes
Liver function
Low serum albumin in nephrotic syndrome
High potassium, low bicarbonate and high phosphate in renal failure
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20
Q

Autoantibodies?

A

ANA
Anti- dsDNA
ANCA
Antiglomerular basement membrane antibodies

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21
Q

Nephritic syndrome (2)?

A
Acute renal failure
Oliguria
Oedema/ fluid retention
Hypertension
Haematuria
Proteinuria <3g/ 24 hours
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22
Q

Nephrotic syndrome?

A
Proteinuria > 3 g/day (mostly albumin, also globulins) 
Can be frothy urine 
Hypoalbuminaemia (<30) 
Oedema
Serum albumin <25g/L
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23
Q

Renal function in nephrotic syndrome?

A

Usually normal

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24
Q

Most common cause of nephrotic syndrome in children?

A

Minimal change disease

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25
Q

What process is indicated in nephrotic syndrome and where is affected?

A

Non- proliferative process

Affects podocytes

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26
Q

Complications of nephrotic syndrome?

A
Infections
Renal vein thrombosis
Pulmonary emboli
Volume depletion 
Vit D deficiency
Subclinical hypothyroidism
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27
Q

Histological classifications in GN?

A

Proliferative/ non- proliferative
Focal/ diffuse
Global/ segmental
Crescentic

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28
Q

Treatment of nephrotic patients?

A
Fluid restriction 
Salt restriction
Diuretics
ACEI/ ARB
Anticoagulation
IV albumin (if volume deplete)
Immunosuppression
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29
Q

What is the aim of treatment in nephrotic patients?

A
Induce sustained remission
Complete remission (proteinuria <300mg/ day)
Partial remission (proteinuria <3g/ day)
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30
Q

Main types of idiopathic GN ?

A
Minimal change
FSGS
Membranous
Membranoproliferative
IgA nephropathy
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31
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change nephropathy

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32
Q

Who gets minimal change nephropathy?

A

Children 2- 4

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33
Q

Renal biopsy on light microscopy and immunofluorescence in minimal change nephropathy?

A

Normal

Negative IF

34
Q

Electron microscopy in minimal change nephropathy?

A

Widespread fusion of epithelial cell foot processes on outside of glomerular basement membrane

35
Q

Clinical features of minimal change nephropathy?

A
Nephrotic syndrome with selective proteinuria
normal renal function
Normal BP
Normal complement
Inc risk of infections
36
Q

What is minimal change nephropathy associated with?

A

Atopy in children - HLA- DR7 positive

37
Q

Treatment for minimal change nephropathy?

A

Oral steroids (prednisolone)

38
Q

Second line drugs in minimal change nephropathy?

A

Cyclophosphamide/ CSA or ciclosporin

39
Q

Does minimal change nephropathy cause progressive renal failure

A

No my breh

40
Q

FSGS?

A

Focal segmental glomerulosclerosis

41
Q

What is the commonest cause of nephrotic syndrome in adults?

A

FSGS

42
Q

Renal biopsy in FSGS?

A

Light microscopy - minimal Ig/

Complement deposition on

43
Q

What may FSGS be associated with?

A

Haematuria
Hypertension
Impaired renal function

44
Q

Treatment of FSGS?

A

4 months high dose prednisolone

If unsuccessful -> addition of cyclophosphamide or ciclosporin

45
Q

How many with FSGS progress to ESRF?

A

50%

46
Q

Collapsing glomerulopathy?

A

Associated with HIV

47
Q

2nd commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy

48
Q

what occurs in membranous nephropathy?

A

Widespread thickening of glomerular basement membrane

49
Q

Who is more at risk of getting membranous nephropathy?

A

Men

50
Q

What may membranous nephropathy present with?

A

Protineuria or nephritic syndrome, hypertension

51
Q

2nd degree causes of membranous nephropathy?

A

Infections (hep B/ parasites)
Connective TD (SLE)
Malignancies (carcinoma/ lymphoma)
Drugs (gold/ penicillamine)

52
Q

Renal biopsy in membranous nephropathy?

A

Subepithelial immune complex deposition in basement membrane

53
Q

What may the idiopathic form of membranous nephropathy respond to?

A

Alternate months of corticosteroids with chlorambucil or cyclophosphamide, or to ciclosporin

54
Q

Appearance of membranous nephropathy?

A

Thick membranes
Sub- epithelial immune deposits
Silver stain -> spikes

55
Q

Membranoproliferative/ mesangiocapillary glomerulonephritis (MCGN)?

A

Proliferation of mesangial cells, inc in mesangial matrix and thickening of glomerular basement membrane

56
Q

How may MCGN present?

A

Nephritic or nephrotic syndrome in young adults or children

57
Q

What is MCGN associated with?

A

Low levels of C3

58
Q

Appearance of MCGN?

A

Big lobulated hyper cellular glomeruli with thick membranes

Tram tracks

59
Q

How many with MCGN develop ESRD?

A

~50%

60
Q

Treatment of MCGN?

A

Nephrotic its with corticosteroids (no proven benefit)

61
Q

What is IgA nephropathy?

A

Asymptomatic microhaematuria +/- non- nephrotic range proteinuria
Genetically abnormal IgA

62
Q

Cause of IgA nephropathy?

A

Genetic
Acquired defect e.g. coeliac
Post infectious

63
Q

Who gets IgA nephropathy?

A

Post infection

64
Q

Is IgA nephropathy nephritic or nephrotic?

A

Nephritic

65
Q

Appearance of IgA nephropathy?

A

IgA deposition in mesangium

66
Q

Presentation of IgA nephropathy?

A

Macroscopic Haematuria after resp/ GI infection

67
Q

What is IgA nephropathy associated with?

A

Henoch-Schonlein Purpura (HSP) (arthritis/colitis/ purpuric skin rash)

68
Q

Renal biopsy in IgA nephropathy?

A

Mesangial cell proliferation and expansion on light microscopy with IgA deposits in mesangium on IF

69
Q

Kidneys in IgA nephropathy?

A

AKI/ CKD

70
Q

How many with IgA nephropathy progress to ESRF?

A

~25%

71
Q

Treatment for IgA nephropathy?

A

BP control/ ACEI or ARB/ fish oil

72
Q

Rapidly progressive glomerulonephritis? (RPGN)

A

Treatable cause of renal failure
Rapid deterioration in renal function over days/ weeks
Active urinary sediment (RBC, RBC and granular casts)

73
Q

What may RPGN be part of?

A

Systemic disease

74
Q

What is RPGN associated with?

A

Glomerular crescents on biopsy

75
Q

Treatment for RPGN?

A

Prompt immunosuppression
Steroids (IV methylprednisolone/ oral prednisolone)
Cytotoxics (cyclophosphamide/ mycophenalate/ azathioprine)
Plasmapharesis

76
Q

Good pastures syndrome?

A

Due to antibodies directed against alpha 3 chain of type IV collagen

77
Q

What is type IV collagen a structural component of?

A

Glomerular basement membrane

78
Q

What do 50% patients with good pastures have?

A

Pulmonary haemorrhage

79
Q

Presentation of good pastures?

A

Rapidly progressive glomerulonephritis

Usually leading to renal failure if untreated

80
Q

Treatment of Goodpastures?

A

Prednisolone
Cyclophoshphamide
Plasma exchange

81
Q

Salt losing nephropathy?

A

Renal loss of sodium
Leads to hyponatraemia and ECV loss
Sometimes after UTI

82
Q

Acute tubulointerstitial nephritis?

A

Patient started on new drug
Symptoms of fever, rash, urine abnormalities
Prednisolone