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Renal/Urology > Lecture 13 - Glomerular Diseases (clinical) > Flashcards

Lecture 13 - Glomerular Diseases (clinical) Flashcards

1
Q

What are glomerular diseases?

A

Inflammatory disorders of the kidney

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2
Q

What are glomerular diseases classified on? What investigation is necessary to differentiate them?

A

Morphology

Biopsy

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3
Q

What are the typical clinical features of a glomerulonephritis?

A

Haematuria
Proteinuria
Hypertension
Renal insufficiency

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4
Q

What are the types of haematuria?

A

Macroscopic/franks vs microscopic

Persistent vs transient

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5
Q

Define microscopic haematuria

A

5+ RBC per high power field

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6
Q

Is haematuria more typical of nephrotic or nephritic syndrome?

A

Nephritic

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7
Q

What can be the sources of blood in haematuria?

A

Kidney, ureter, bladder, urethra, prostate

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8
Q

What kind of haematuria do you tend to see in glomerulonephritis?

A

Persistent macroscopic haematuria (microscopy shoes dysmorphic RBCs)

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9
Q

Where abouts is the problem if you have proteinuria?

A

Glomerulus/tubules

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10
Q

How can you measure proteinuria?

A

Urine protein creatinine ratio

24 hour urine collection

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11
Q

What kind of proteinuria do you tend to see in glomerulonephritis?

A

Persistent proteinuria of more than 1g/mmol creatinine

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12
Q

Is hypertension more typical of nephritic or nephrotic syndrome?

A

Nephritic

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13
Q

What features are typical of nephritic syndrome?

A 
Haematuria
Mild/moderate proteinuria
Hypertension 
Oliguria
Red cell casts in the urine
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14
Q

What features are typical of nephrotic syndrome?

A

Oedema
Proteinuria >3.5g/day
Hypoalbuminaemia (<30g/L)
Hyperlipidaemia

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15
Q

What will you see on urinalysis of someone with nephrotic syndrome?

A

Proteinuria (protein ++++)

Frothy appearance

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16
Q

Why are individuals with nephrotic syndrome predisposed to thrombosis?

A

Loss of antithrombin III, proteins C and S and associated rise in fibrinogen levels

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17
Q

What are differential diagnoses for nephrotic syndrome and how could you differentiate them from nephrotic syndrome?

A

Congestive heart failure (JVP raised, normal albumin, minimal proteinuria)

Hepatic disease (abnormal LFTs, no proteinuria)

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18
Q

What are the aetiologies of glomerulonephritis?

A

Autoimmune
Infection
Malignancy
Drugs

NB same diseases can be caused by different things

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19
Q

What are the two subtypes of GNs?

A

Proliferative

Non-proliferative

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20
Q

What is a proliferative GN?

A

One in which there are excessive numbers of cells in glomeruli, incl infiltrating leucocytes

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21
Q

What is a non-proliferative GN?

A

Glomeruli appear normal or have areas of scarring

Normal number of cells

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22
Q

What is meant by a diffuse GN?

A

> 50% glomeruli affected

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23
Q

What is meant by a focal GN?

A

<50% of glomeruli affected

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24
Q

What is meant by a global GN?

A

All glomerulus affected

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25
Q

What is meant by a segmental GN?

A

Part of glomerulus affected

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26
Q

What GNs cause a nephrotic syndrome?

A

Minimal change disease

Membranous nephropathy

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27
Q

What GNs cause a nephritic state?

A

ANCA associated GN
Post-infectious GN
Crescentic GN
Diffuse proliferative GN

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28
Q

What GN largely just causes proteinuria and urinary sediment abnormalities?

A

IgA nephropathy

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29
Q

What GNs can cause nephrotic/nephritic state?

A

FSGS

Mesangioproliferative GN

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30
Q

List 4 of the proliferative GNs

A

Diffuse proliferative - post-infective nephritis
Focal proliferative - mesangial IgA
Focal necrotizing (crescentic) nephritis
Membrano-proliferative nephritis

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31
Q

What nodules do you see in post-infectious GN?

A

Kimmersteil-Wilson nodules

May also see IgA deposits

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32
Q

What is the natural history of post-strep GN?

A

Follows 10-21d post throat/skin infection

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33
Q

What organism most commonly causes post-strep GN?

A

Lancefield group A strep (usually strep pyogenes)

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34
Q

What alleles genetically predispose someone to getting post-strep GN?

A

HLA-DR, -DP

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35
Q

What causes post-strep GN?

A

Immune complexes (IgG, IgM, C3) deposition in the glomeruli

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36
Q

Who is most affected by post-strep GN?

A

Young children usually

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37
Q

What are the clinical features of post-strep GN?

A 
Headache, malaise
Haematuria
Proteinuria
HTN
Low C3
Raised ASO titre
1-2w post URTI
(more nephritic state, e.g. red cell casts etc)
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38
Q

How is post-strep GN treated?

A

Vasodilator drugs, e.g. amlodipine for HTN

Loop diuretics, e.g. frusemide if any oedema

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39
Q

What is the commonest GN worldwide?

A

IgA nephropathy

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40
Q

What characterises IgA nephropathy?

A

IgA deposition in the mesangium + mesangial proliferation

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41
Q

Who most commonly gets IgA nephropathy?

A

20-30 yo males

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42
Q

What % of cases of IgA nephropathy progress to ESRD?

A

40%

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43
Q

How can IgA nephropathy present?

A

Microscopic haematuria (can be silent for a while)
Microscopic haematuria + proteinuria
Nephrotic syndrome
IgA crescentic GN

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44
Q

What is IgA nephropathy AKA?

A

Berger’s disease

45
Q

How does IgA nephropathy classically present?

A

Macroscopic haematuria in young people following an URTI

typically nephritic syndrome!

46
Q

What conditions are associated with IgA nephropathy?

A

Alcoholic cirrhosis
Coeliac disease/dermatitis herpetiformis
HSP

47
Q

What do you see on histology in IgA nephropathy?

A

Mesengial hypercellularity

Positive immunofluorescence for IgA + C3

48
Q

What is a marker of good prognosis in IgA nephropathy?

A

Frank haematuria

49
Q

What is a marker of poor prognosis in IgA nephropathy?

A 
Male grnder
Proteinuria (esp >2g/day)
HTN
Smoking
Hyperlipidaemia
ACE genotype DD
50
Q

What are the types of crescentic GN?

A

ANCA associated: microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis

Anti-GBM - e.g. anti-GBM nephritis or Goodpasture’s syndrome

Others - IgA vasculitis, post-infection GN, SLE

51
Q

What is goodpastures syndrome?

A

A rare condition associated with pulmonary haemorrhage and rapidly progressive GN

52
Q

What causes goodpastures syndrome?

A

Anti-glomerular basement membrane antibodies against type IV collagen

53
Q

What HLA allele is associated with goodpastures syndrome?

A

HLA DR2

54
Q

What factors in goodpastures syndrome increase the likelihood of pulmonary haemorrhage?

A 
Smoking
LRTI
Pulmonary oedema
Inhalation of hydrocarbons
Young male
55
Q

How do you investigate suspected goodpasture syndrome?

A

Renal biopsy (linear IgG deposits along the basement membrane)

56
Q

What is involved in the management of goodpastures syndrome?

A

Plasmapheresis
Steroids
Cyclophosphamide

57
Q

What causes anti-GBM disease?

A

Circulating anti-GBM antibodies

58
Q

How can anti-GBM present?

A

Nephritis - anti-GBM glomerulonephritis

Nephritis + lung haemorrhage (Goodpastures)

59
Q

How is anti-GBM disease treated?

A

Aggressive immunosuppression - steroids, plasma exchange, cyclophosphamide

60
Q

How is crescentic GN managed?

A

Corticosteroids, plasma exchange, cyclophosphamide, B cell therapy (e.g. rituximab), complement inhibitors

61
Q

What does 10-20% of anti-GBM disease progress to?

A

Crescentic GN

62
Q

How do proliferative GNs present?

A

Nephritic syndrome

63
Q

What are the main non-proliferative GNs?

A

Minimal change disease
Focal and segmental GN
Membranous nephropathy

64
Q

How is nephrotic syndrome managed?

A

Treat oedema –> fluid + salt restriction, loop diuretics
HTN: RAAS blockade
Reduce risk thrombosis: heparin/warfarin
Reduce risk of infection e.g. pneumococcal vaccine
Treat dyslipidaemia, e.g. with statins

65
Q

Who is minimal change disease the most common GN in?

A

Children

66
Q

How does minimal change disease tend to present?

A

Sudden onset oedema (nephrotic syndrome)

67
Q

How is minimal change disease treated?

A

Steroids (prednisolone 1mg/kg for up to 16w, taper over 6m once remission achieved)

68
Q

What fraction of pts with minimal change disease relapse?

A

2/3rd

69
Q

If someone has a relapse of minimal change disease how is this managed?

A 
Cyclophosphamide
Cyclosporin
Tacrolimus
Mycophenolate mofetil
Rituximab
70
Q

What is the prognosis of minimal change disease?

A

1/3 - just one episode
1/3 - infrequent episodes
1/3 - frequent episodes which stop before adulthood

71
Q

Does minimal change disease present as a nephrotic or nephritic syndrome?

A

Nephrotic

72
Q

What are the aetiologies for minimal change disease?

A

Usually idiopathic
Drugs: NSAIDs, rifampicin
Hodgkin’s lymphoma, thymoma
IM

73
Q

What is the pathophysiology of minimal change disease?

A

T-cell and cytokine mediated damage to the glomerular basement membrane –> polyanion loss
Resultant reduction of electrostatic change –> increased glomerular permeability to albumin

74
Q

What are the features of minimal change syndrome?

A

Nephrotic syndrome

Highly selective proteinuria (only medium sized proteins, e.g. albumin + transferrin)

75
Q

What do you see on renal biopsy in minimal change disease?

A

Normal glomeruli on light microscopy

Electron microscopy shows fusion of podocytes + effacement of foot processes

76
Q

What % of minimal change disease is steroid responsive?

A

80%

Cyclophosphamide next step for steroid resistant cases

77
Q

What is focal and segmental GN?

A

A syndrome with multiple causes

78
Q

Does focal and segmental GN present with a nephritic or nephrotic syndrome?

A

Nephrotic

79
Q

What do you see on histology in focal and segmental GN?

A

Focal + segmental sclerosis with distinctive patterns, e.g. tip lesion, collapsing, cellular etc.

80
Q

Can focal and segmental GN be treated with steroids?

A

No - usually v. steroid resistant

81
Q

What is the prognosis of focal and segmental GN?

A

High chance of progression to ESRD

82
Q

How is focal and segmental GN managed?

A

General measures for nephrotic syndrome, e.g. treat oedema, HTN etc.
Trial steroids, even if partial remission
Alt options: cyclophosphamide, cyclosporin, rituximab

83
Q

What is focal and segmental GN aka?

A

Focal segmental glomerulosclerosis

84
Q

Who does FSGS normally present in?

A

Young adults

85
Q

What are causes of FSGS?

A 
Idiopathic
2 to other renal pathology, e.g. IgA nepropathy, reflux nephropathy
HIV
Heroin
Alport's syndrome
Sickle-cell
86
Q

What is the recurrence rate of FSGS like post-transplant?

A

V. high

87
Q

What do you see on renal biopsy in FSGS?

A

Focal + segmental sclerosis + hyalinosis on light microscopy

Effacement of foot processes on electron microscopy

88
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy (usually idiopathic)

89
Q

What antibody is present in 70% cases of membranous nephropathy?

A

Anti-phospholipase A2 receptor antibody

90
Q

What are secondary causes of membranous nephropathy?

A 
Malignancies - lung cancer, lymphoma, leukaemia
SLE
RA
Infections - hep B, malaria, syphillis
Drugs - NSAIDs, gold, penicillamine
91
Q

What other marker is screened for in membranous nephropathy (apart from PLA2R)?

A

Thrombospondin type 1 domain containing 7A

92
Q

What can you see on electromicroscopy in membranous nephropathy?

A

Basement membrane is thickened with subepithelial electron dense deposits - creates a spike and dome appearance

93
Q

How is membranous nephropathy managed?

A

ACEi/ARB
General measures for at least 6m
Immunosupression if severe/progressive disease
Corticosteroids tend to be used in combo with another agent, e.g. cyclophosphamide
Anticoagulation for high risk pts

94
Q

What is the prognosis of membranous nephropathy?

A

1/3rd: spontaneous remission
1/3rd remain proteinuric
1/3rd develop ESRD

95
Q

What is membranoproliferative GN AKA?

A

Mesangiocapillary GN

96
Q

How can membranoproliferative GN present?

A

Nephrotic syndrome, haematuria or proteinuria

97
Q

What is the prognosis of membranoproliferative GN?

A

Poor

98
Q

What the different types of membranoproliferative GN?

A

Type 1
Type 2
Type 3

99
Q

What is the most common type of membranoproliferative GN?

A

Type 1 (90%)

100
Q

What are the causes of type 1 membranoproliferative GN?

A

Cryoglobinaemia

Hepatitis C

101
Q

What do you see on electromicroscopy on membranoproliferative GN?

A

Subendothelial and mesangium immune desposits of electron dense material –> tram track appearance

102
Q

What is type 2 membranoproliferative GN?

A

Dense deposit disease
Caused by persistent activation of alternative complement pathway
Causes - partial lipodystrophy, factor H deficiency

103
Q

What blood result abnormality do you see in patients with type 2 membranoproliferative GN?

A

Low circulating levels of C3

104
Q

What do you see on electron microscopy in type 2 membranoproliferative GN?

A

Intramembranous immune complex deposits with dense deposits

105
Q

What are causes of type 3 membranoproliferative GN?

A

Hep B and C

106
Q

How can membranoproliferative GN be treated?

A

Steroids may be effective

107
Q

What is rapidly progressive GN?

A

Term used to describe a rapid loss of renal function assoc. w formation of epithelial crescents in the majority of glomeruli

108
Q

What are causes of rapidly progressive GN?

A

Goodpastures syndrome
Wegner’s granulomatosis
SLE, microscopic polyarteritis

109
Q

What are features of rapidly progressive GN?

A

Nephritic syndrome + features specific to underlying cause, e.g. vasculitis rash and sinusitis with Wegners

Renal/Urology (29 decks)

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