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Renal Pathology > Glomerular Disease > Flashcards

Glomerular Disease Flashcards

1
Q

How does blood enter to the glomerulus?

A

Via the afferent arteriole

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2
Q

What will NOT be filtered by the glomerulus and will stay in the plasma?

A

All proteins equal to or larger than albumin (including immunoglobulins)

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3
Q

Layers of the filter barrier

A
  1. Endothelial cell cytoplasm
  2. Basal lamina
  3. Podocytes
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4
Q

How many layers does the glomerular membrane / filter have?

A

3

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5
Q

What are mesangial cells?

A

Tree like group of cells (pericytes) which support capillaries

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6
Q

Where does filtrate go?

A

Into bowmans space then into the proximal tubule

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7
Q

What does the efferent arteriole contain?

A

Plasma

Unfiltered proteins e.g. albumin and antibodies

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8
Q

Classification of glomerulonephritis

A

Primary

Secondary

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9
Q

What is primary glomerulonephritis?

A

Only affects the glomerulus

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10
Q

What is secondary glomerulonephritis?

A

Other parts of the body are affected also e.g. Wegeners, SLE

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11
Q

What is glomerulonephritis a disease of?

A

The glomerulus

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12
Q

What are the 4 presentations of glomerulonephritis?

A

Haematuria
Heavy proteinuria (causing nephrotic syndrome). Very suddenly comes on
Slowly increasing proteinuria
Acute renal failure

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13
Q

Definition of haematuria

A

Blood in urine

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14
Q

4 most common causes of haematuria (in order of most to least common)

A
  1. UTI
  2. Urinary tract stone +/- infection
  3. Urinary tract tumour
  4. Glomerulonephritis
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15
Q

What must always be checked before a renal biopsy?

A

Clotting

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16
Q

Types of glomerulonephritis

A

IgA Glomerulonephritis
Membranous Glomerulonephritis
Diabetic Nephropathy
Crescentic Glomerulonephritis

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17
Q

Presentation of IgA Glomerulonephritis

A

Discoloured urine - dipstick +ve for blood

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18
Q

What would be seen in IgA Glomerulonephritis on kidney biopsy?

A

IgA immunoglobulins and complement C3 in mesangial area of all glomeruli

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19
Q

What would be seen in IgA glomerulonephritis on electron microscopy?

A

Deposits of IgA with prominent mesangial cells

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20
Q

Is there excess antibody produced in IgA glomerulonephritis?

A

Sometimes present in the serum however this is also sometimes true for people without the IgA glomerulonephritis - so no

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21
Q

Pathology of IgA glomerulonephritis

A

IgA gets stuck within the mesangium

IgA irritates the mesangial cells and causes them to proliferate and produce more matrix

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22
Q

Prognosis of IgA nephropathy

A

Usually self limiting i.e. return to normal

Small % go onto chronic renal failure due to continued deposition of the matrix

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23
Q

Presentation of membranous glomerulonephritis

A 
Feeling generally unwell 
Swollen legs 
Low albumin 
Dipstick proteinuria 
Haematuria
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24
Q

Pathology of membranous glomerulonephritis

A

Thickened glomerular basement membrane
Spikes of new basement membrane matrix material underneath podocytes (matrix tries to surround and remove the deposit)
Deposit of IgG. IgG is too big to be filtered into the urine but activates complement (C3) which punches holes in the filter.
Damage to basal lamina
End up with leaky basal lamina - leaking albumin into the urine (nephrotic syndrome)

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25
Q

Is albumin filtered out of the plasma?

A

No

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26
Q

What is stuck in the membrane in membranous glomerulonephritis?

A

IgG

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27
Q

Prognosis of membranous glomerulonephritis

A

1/4 chronic renal failure within 10 years

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28
Q

What would be seen on a renal biopsy in diabetic nephropathy?

A

Glycated molecules -> matrix deposition in basal lamina underlying endothelium and in mesangial matrix -> thickened but leaky basement membranes and mesangial matrix compresses capillaries (no immune complexes)

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29
Q

Pathology of diabetic nephropathy

A

Thickened capillary wall which is leaking albumin
Increased mesangial matrix (which compresses capillaries)
Thickened, narrowed arterioles reduce blood flow to the glomerulus
Adhesions to Bowmans capsule are glomerulus attempt to stop massive leakage of albumin into the urine
Gross excess of mesangial matrix forming nodules

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30
Q

What are the nodules of the mesangial matrix in diabetic nephropathy called?

A

Kimmel-steil Wilson Lesion

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31
Q

When is there inevitable decline of diabetic nephropathy?

A

Established diabetic nephropathy
AND
Continued poor glycaemic control

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32
Q

What does rapidly rising creatinine indicate?

A

Acute renal failure

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33
Q

Pathology of crescentic glomerulonephritis

A

Cellular proliferation and influx of macrophages (=crescent) around glomerular tuft, within bowmans space
Endothelial damage with fibrin deposition
Crescent often ends up with a C shape

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34
Q

Causes of the pattern of injury seen in crescentic glomerulonephritis

A

Wegeners granulomatosis
Microscopic polyarteriits
Antiglomerular basement membrane disease
Other forms of glomerulonephritis

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35
Q

What is another name for wegeners granulomatosis?

A

Granulomatosis with polyangitis

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36
Q

What is wegeners granulomatosis?

A

A form of vasculitis which affects the vessels in kidneys, nose and lungs

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37
Q

Definition of vasculitis

A

Primary inflammation of the vessels

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38
Q

Investigation for wegeners

A

Serum ANCA

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39
Q

What does ANCA stand for?

A

Anti-neutrophil cytoplasmic antibodies

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40
Q

Is ANCA deposited in the kidney?

A

No

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41
Q

How does ANCA cause damage?

A

Antibodies directed against proteinase 3 and myeloperoxidase, 2 enzymes in primary granules of neutrophils
Antibodies product tissue damage via interactions with primed neutrophils and endothelial cells

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42
Q

Prognosis of wegeners

A

Fatal (mean survival 6 months) if untreated

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43
Q

Treatment of wegeners

A

Cyclophosphamde (chemotherapy) - 75% complete remission

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44
Q

Types of haematuria

A

Macroscopic

Microscopic

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45
Q

What is macroscopic haematuria?

A

Tea or cold coloured or frank blood in the urine

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46
Q

What is microscopic haematuria?

A

> 5 RBCs per high power field

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47
Q

What can be the source of haematuria?

A 
Kidney 
Ureter
Bladder
Prostate
Urethra
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48
Q

What type of haematuria is seen in glomerulonephritis?

A

Persistent microscopic haematuria

Microscopy shows dysmorphic RBCs (mickey-mouse like)

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49
Q

Types of proteinuria

A

Glomerular or tubular

Albumineria or proteinuria

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50
Q

Which of nephritis and nephrotic syndrome presents with haematuria more?

A

Nephritis > nephrotic

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51
Q

Which one of nephritis or nephrotic syndrome presents with haematuria more?

A

Nephritis = Nephrosis

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52
Q

What type of proteinuria is present in glomerulonephritis?

A

Persistent

Proteinuria of more than 1 gram/mmol creatinine

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53
Q

What % of end stage kidney disease does glomerulonephritis make up?

A

30%

54
Q

What is glomerulonephritis classified based on?

A

Morphology

55
Q

What are the majority of glomerulonephritis attributed to?

A

Autoimmune aetiologies

56
Q

Features of glomerulonephritis

A

Haematuria
Proteinuria
Hypertension
Renal insufficiency

57
Q

Which of nephrotic syndrome and nephritic syndrome is there mostly HTN?

A

Nephritis > Nephrotic

58
Q

Features of the nephritic state

A 
Active urine sediment 
- haematuria
- dysmorphic RBCs
- cellular casts
HTN
Renal impairment
59
Q

Features of nephrotic state

A

Oedema
Proteinuria >3.5g/day
Hypoalbuminemia
Hyperlipidaemia

60
Q

Differential diagnosis of nephrotic syndrome

A 
CHF (raised JVP, normal albumin, minimal proteinuria)
Hepatic disease (abnormal LFTs, no proteinuria)
61
Q

Causes of glomerulonephritis

A 
Autoimmune
Infection 
Malignancy 
Drugs
Others
62
Q

Types of glomerulonephritis

A

Primary; kidney alone

Secondary; part of a multisystem disease

63
Q

Morphological types of glomerulonephritis

A

Proliferative

Non-proliferative

64
Q

Features of proliferative glomerulonephritis

A

Excessive numbers of cells in glomeruli - these include infiltrating leucocytes

65
Q

Features of non proliferative glomerulonephritis

A

Glomeruli look normal or have areas of scarring

They have normal numbers of cells

66
Q

What can nephrotic syndrome cause?

A

Minimal change disease

Membranous nephropathy

67
Q

What can nephritic state cause?

A

ANCA associated glomerulonephritis

Post infection glomerulonephritis

68
Q

Is minimal change disease caused by nephrotic or nephritic disease?

A

Nephrotic

69
Q

Is diffuse proliferative GN and crescenteric GN more nephrotic or nephritic?

A

Nephritic

70
Q

Is membranoproliferative GN more nephrotic or nephritic?

A

Nephrotic 2 > 3 Nephritic

71
Q

Is mesangioproliferative GN more nephrotic or nephritic?

A

Both the same

72
Q

Examples of proliferative glomerulinephritis

A

Diffuse proliferative - post infection nephritis
Focal proliferative - mesangial IgA disease
Focal necrotising (crescentic) nephritis
Membrano-proliferative nephritis

73
Q

Treatment of post infective glomerulonephritis

A

Antibiotics for infection
Loop diuretics such as furesimide for oedema
Vasodilator drugs (e.g. amlodipine) for HTN

74
Q

When does post-streptococcal glomerulonephritis occur?

A

10 - 21 days after an infection typically of throat or skin

75
Q

What is the post streptococcal glomerulonephritis most common organism?

A

Lancefield Group A streptococci

76
Q

What is the genetic predisposition to post strep glomerulonephritis?

A

HLA-DR

77
Q

What is the most common cause of glomerulonephritis worldwide?

A

IgA nephropathy

78
Q

Pathology of IgA Nephropathy

A

IgA deposition in the mesangium and mesangial proliferation

79
Q

What decade of life does IgA nephropathy present? What gender?

A

2nd and 3rd

M > F

80
Q

What % of IgA nephropathy can progress to end stage kidney disease?

A

40%

81
Q

Presentation of IgA nephropathy

A

Microscopic haematuria
Microscopic haematuria + proteinuria
Nephrotic syndrome
IgA Crescentic glomerulonephritis

82
Q

Treatment for Focal necrotising glomerulonephritis

A

High dose steroids
Cyclophosphamide
Plasma exchange

83
Q

Treatment of crescentic glomerulonephirits

A

Immunosuppression

  • corticosteriods
  • plasma exchange
  • cyclophosphamide
  • B cell therapy e.g. rituximab
  • complement inhibitors
84
Q

Treatment of crescentric GN

A

High dose steroids
Cyclophosphamide
Plasma exchange

85
Q

What is anti-GMB disease?

A

Rare disease caused by circulating anti-GBM

86
Q

What % of crescenteric glomerulonephritis does anti-GMB make up?

A

10-20%

87
Q

Presentation of anti-GMB disease

A

Nephritis (anti-GMB GN)

Nephritis + lung haemorrhage (goodpastures syndrome)

88
Q

Peak ages for anti-GMB disease

A

3rd decade

89
Q

Investigations for anti-GMB disease

A

Anti-GBM antibodies in serum and kidneys

90
Q

Treatment of anti-GMB disease

A

Aggressive immunosuppression

  • steroids
  • plasma exchange
  • cyclophosphamide
91
Q

What do proliferative GNs present with?

A

Nephritic syndrome

92
Q

Types of non proliferative GN

A

Minimal change disease
Focal and segmental GN
Membranous nephropathy

93
Q

Treatment of nephrotic syndrome

A 
Salt restriction 
Loop diuretics
RAAS blocker
Heparin or warfarin 
Reduce infection e.g. pneumococcal vaccine
Statins
Specific therapy to the cause
94
Q

What is the commonest form of nephrotic syndrome in children?

A

Minimal change

95
Q

Presentation of minimal change disease

A

Sudden onset of oedema - days

Nephrotic syndrome

96
Q

Response of minimal change disease to steroids

A

Complete loss of proteinuria with steroids

97
Q

How many patients with minimal change disease relapse?

A

2/3

98
Q

Treatment of minimal change disease

A 
Prednisolone 1mg/kg for up to 16 weeks
Once remission slow taper over 6 months 
Subsequent relapse can be treated with 
- cyclophosphamide
- cyclosporin 
- tacrolimus
- mycophenolate mofetil 
- rituximab
99
Q

Prognosis of minimal change disease

A

Despite relapsing behaviour, prognosis Is favourable
Risk of end stage kidney disease is low
Steriods toxicity as multiple exposure

100
Q

What is focal and segmental GN?

A

Not a single disease, a syndrome with multiple causes

101
Q

What does focal and segmental GN present with?

A

Nephrotic syndrome

102
Q

Histology of focal and segmental GN

A

Tip lesion
Collapsing
Cellular
Perihillar

103
Q

What is an important feature of focal and segmental GN?

A

Steriod resistant

104
Q

Chance of progression of focal and segmental GN to end stage kidney disease

A

High chance

105
Q

Treatment of focal and segmental GN

A 
General measures
Steroids
Alternative
- cyclosporin 
- cyclophosphamide
- rituximab
106
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy

107
Q

Most common cause of membranous nephropathy

A

Idiopathic

108
Q

Serological markers of membranous nephropathy

A

Anti-phospholipase A2 receptor (PLA2R) antibody +ve in 70% of idiopathic cases
Thrombospondin type 1 domain containing 7A (THSD7A)

109
Q

Causes of membraneous nephropathy

A 
Idiopathic
Malignancies
SLE
RA
Drugs
- NSAIDs
- Gold
- Penicillamine
110
Q

Treatment of membraneous nephropathy

A 
General measures for at least 6 months 
Immunosuppression if
- symptomatic nephropathic syndrome
- rising proteinuria 
- deteriorating renal function 
Cyclophosphamide and steroids (alternate months) for 6 months 
Cyclosporine
Rituximab
111
Q

In how many people with membraneous nephropathy resolve spontaneously?

A

1/3

112
Q

What % of patients with membraneous glomerulonephritis are on dialysis at 10 years?

A

25%

113
Q

In what patients can membranous glomerulonephritis can recur?

A

Renal transplants

114
Q

What does non proliferative GN present with?

A

Nephrotic syndrome

115
Q

What is the triad of nephrotic syndrome?

A

Proteinuria
Hypoalbuminuria
Oedema

116
Q

What is minimal change disease very susceptible to?

A

Steriods

117
Q

What is creatinine?

A

A breakdown product from skeletal muscles

118
Q

Is creatinine toxic?

A

Not toxic, just used as a measurement

119
Q

Features of goodpastures syndrome

A

Rapidly progressive GN

Lung haemorrhage

120
Q

Pathology of goodpastures syndrome

A

anti-GBM antibodies against collagen type IV

121
Q

Who gets goodpastures?

A

M > F

20 - 30 + 60 - 70

122
Q

Association of goodpastures

A

HLA-DR2

123
Q

Factors which increase the likelihood of pulmonary haemorrhage

A 
Smoking
LRTI
Pulmonary oedema
Inhalation of hydrocarbons
Young males
124
Q

Investigations of goodpastures

A 
Renal biopsy (linear IgG deposits along basement membranes)
Raised transfer factor (secondary to pulmonary haemorrhages)
125
Q

Management of goodpastures

A

Plasma exchange
Steroids
Cyclophosphamide

126
Q

Post strep GN vs IgA nephropathy WHEN they present

A

IgA - 1 - 2 days after URTI

Post strep - 1 - 2 weeks after URTI

127
Q

Presenting factor (mostly) IgA vs post strep GN

A

IgA - macroscopic haematuria

Post strep - proteinuria

128
Q

What kind of state is membraneous GN?

A

Hypercoagulable state

129
Q

How is nephrotic syndrome a hypercoagulable state?

A

Loss of antithrombin III via the kidneys

130
Q

What is the pneumonic to remember the variables for eGFR and what do they stand for?

A

CAGE

  • creatinine
  • age
  • gender
  • ethnicity

Renal Pathology (13 decks)

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