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Year Two - Urinary System > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What is another term for glomerulonephritis?

A

Intrinsic kidney disease

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2
Q

What is glomerulonephritis?

A

A group of conditions that cause inflammation of or around the glomeruli in the kidney

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3
Q

What is the role of the glomeruli?

A

To remove excess fluid electrolytes and waste from the bloodstream and pass them into urine

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4
Q

What is the glomerulus?

A

A network of capillaries

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5
Q

How does blood enter the glomerulus?

A

Afferent arteriole

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6
Q

What happens as blood passes through the glomerulus?

A

Small molecules are filtered across the glomerular membrane into the Bowman’s space

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7
Q

What molecules are not filtered at the glomerulus? Give an example

A

Molecules which which are too large to filter across the membrane

Albumin

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8
Q

How does unfiltered molecules exit the glomerulus?

A

Efferent arteriole

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9
Q

What are mesanigial cells?

A

They are specialised pericytes within the kidney that make up the mesangium (middle) of the glomerulus

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10
Q

What is the primary function of mesangial cells?

A

To remove trapped residues and aggregated protein from the basement membrane thus keeping the filter free of debris

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11
Q

What is the role of the glomerular filtration barrier?

A

To ensure that large molecules, such as albumin, are unable to escape from the glomerulus into urine

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12
Q

What are the three layers of the glomerular filtration barrier?

A

Endothelium (Inner Layer)

Basal Lamina (Middle Layer)

Podocytes (Outer Layer)

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13
Q

Describe the endothelium that makes up the glomerular filtration barrier

A

It has perforations called fenestrae

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14
Q

What is the function of the endothelium layer of the glomerular filtration barrier?

A

To restrict the filtration of RBC’s

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15
Q

What is the function of the basal lamina layer of the glomerular filtration barrier?

A

To restrict the movement of negatively charged molecules across the basement membrane

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16
Q

Describe the podocyte layer of the glomerular filtration barrier

A

There are foot-like processes projecting from podocytes that interdigitate to form filtration slits

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17
Q

What is the pathophysiological cause of glomerulonephritis?

A

It occurs when there is damage to the glomerular filtration barrier, resulting in the leakage of RBC’s and albumin

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18
Q

What are the five clinical features of glomerulonephritis? Why?

A

Haematuria, which is the presence of blood within urine resulting in pink-coloured urine

Proteinuria, which is the presence of more than 1.5g (150mg) of protein within urine per day, resulting in foamy urine

Hypertension, which is high blood pressure

Oedema, which specifically affects the patient’s face, hands, feet and abdomen

Oliguria, which is the defined as a decreased urine output – specifically less than 0.5ml/kg/hour

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19
Q

What are the three types of haematuria?

A

Visible

Microscopic

Dipstick positive

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20
Q

Why is proteinuria a clinical feature of glomerulonephritis?

A

This is due to the fact that proteins can pass through the triple filtration barrier and into urine

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21
Q

Why is hypertension a clinical feature of glomerulonephritis?

A

This is due to the fact that salt and water are retained within blood

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22
Q

Why is oedema a clinical feature of glomerulonephritis?

A

This is due to the retention of fluid

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23
Q

Why is oliguria a clinical feature of glomerulonephritis?

A

This is due to the retention of fluid

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24
Q

What is nephritic syndrome?

A

A group of clinical features which reflect inflammation of the kidney

It doesn’t represent a specific syndrome or underlying cause

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25
Q

Are there set criteria a patient must met in order to have nephritic syndrome?

A

No, instead the patient just presents with the clinical features of glomeruloneprhtiis

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26
Q

What is a prominent clinical feature of nephritic syndrome?

A

Proteinuria

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27
Q

What is the pathophysiological cause of nephritic syndrome?

A

It is caused by the invasion of inflammatory cells into the glomerulus

These inflammatory cells then attack the triple filtration barrier, resulting in the leakage of RBCs and some albumin.

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28
Q

What is a prominent clinical feature of nephrotic syndrome? What is not a prominent clinical feature of nephrotic syndrome?

A

Haematuria

Proteinuria

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29
Q

What are the four criteria of nephrotic syndrome?

A

Peripheral Oedema

Proteinuria, which is defined as >3.5g per 24hrs

Hypoalbuminemia, which is defined as serum albumin <35g/L

Hypercholesterolaemia, which is defined blood cholesterol > 200mg/dl

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30
Q

What is the pathophysiological cause of nephrotic syndrome?

A

It is caused by podocytes and their foot processes separating, thus resulting in leakage of albumin and some RBCs

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31
Q

What are the two main classifications of glomerulonephritis?

A

Proliferative Glomerulonephritis

Non-Proliferative Glomerulonephritis

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32
Q

What is proliferative glomerulonephritis?

A

It is characterised by increased cellularity of the glomerulus

This is due to the invasion of inflammatory cells

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33
Q

What are the four subclassifications of proliferative glomerulonephritis?

A

IgA nephropathy

Membranoproliferative Glomerulonephritis

Diffuse Proliferative Glomerulonephritis

Crescentic Glomerulonephritis

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34
Q

Is proliferative glomerulonephritis nephrotic or nephritic?

A

Nephritic

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35
Q

What is the most common glomeurlonephritis classification?

A

IgA nephropathy

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36
Q

What are another two terms for IgA nephropathy?

A

Mesangioproliferative glomerulonephritis

Berger’s disease

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37
Q

What is IgA nephropathy?

A

It is characterised by a mesangial deposition of IgA immune complexes

38
Q

In which patient group does IgA nephropathy tend to present in?

A

Male patients

Between the ages of 20 – 30 years old

39
Q

What are the three risk factors of IgA nephropathy?

A

Alcoholic cirrhosis

Coeliac disease

Hence Schonlein purpura

40
Q

How does mesangioproliferative gloumerulonephritis tend to present?

A

Macroscopic haematuria

Following an upper respiratory tract infection

41
Q

How are the two features of IgA nephropathy on histological examination?

A

Mesangial hypercellularity

Positive immunofluorescence for IgA & C3

42
Q

What is the conservative management of IgA nephropathy?

A

No treatment

Follow up to check renal function

43
Q

When do we recommend conservative management of IgA nephropahty?

A

In cases of isolated haematuria, with no proteinuria and a normal GFR

44
Q

What are the two pharmacological management options of IgA nephropathy?

A

ACE inhibitors

Corticosteroids

45
Q

When are ACE inhibitors used to manage IgA nephropathy?

A

In cases of persistent proteinuria > 500 - 1000mg/day, with a normal or only slightly reduced GFR

46
Q

When are corticosteroids used to manage IgA nephropathy?

A

In cases where there is failure to respond to ACE inhibitors or GFR levels are reduced

47
Q

What are the three differences between IgA nephropathy and post-streptococcal glomerulonephritis?

A

IgA nephropathy = high complement levels, haematuria, onset of features following infection is 1-2 days

Post-streptococcal glomerulonephritis = low complement levels, proteinuria, onset of features following infection is 1-2 weeks

48
Q

How do we diagnose mesangioproliferative glomerulonephritis?

A

The IgA deposits are not filtered into the urine

An elevated level of IgA is only identified within blood

49
Q

What is membranoproliferative glomerulonephritis ?

A

It is characterised by an increased number of cells within the glomerular basement layer of the glomeruli

50
Q

What is another term for diffuse proliferative glomerulonephritis?

A

Post infectious glomerulonephritis

51
Q

What is diffuse proliferative glomerulonephritis?

A

A severe form in which proliferative changes occur in more than 50% of the glomeruli

52
Q

In which patient group does diffuse proliferative glomerulonephritis tend to present in?

A

Younger patients

One to three weeks after an infection of the throat or skin, such as tonsilitis or impetigo

53
Q

What organism tends to cause diffuse proliferative glomerulonephritis?

A

Lancefield group A streptococci

54
Q

Why do infections cause diffuse proliferative glomerulonephritis?

A

In order to fight the infection, the body produces extra antibodies that can eventually settle in the glomeruli, causing inflammation and thus glomerulonephritis

55
Q

What is crescentic glomerulonephritis?

A

It is characterised by the formation of glomerular crescents within the glomeruli

This crescent is formed as a result of cellular proliferation and macrophage influx within the Bowman’s space

56
Q

What are the two subclassifications of crescentic glomerulonephritis?

A

ANCA-Associated Glomerulonephritis

Anti-GBM Nephritis

57
Q

What is ANCA associated glomerulonephritis?

A

It is a condition in which ANCA vasculitis of the lungs starts to affect the kidneys

58
Q

How do ANCA antibodies cause ANCA associated glomerulonephritis?

A

ANCA antibodies are directed against two neutrophilic enzymes – proteinase 3 and myeloperoxidase.

Therefore, when inflammation occurs and neutrophils infiltrate the glomerulus, a high production of ANCA antibodies occurs which then causes tissue damage within the kidney.

59
Q

What is another name for anti-GMB nephritis?

A

Goodpasture’s syndrome

60
Q

What is anti-GMB nephritis?

A

It is a condition in which anti-GMB antibodies attack the basement membranes of the glomerulus and lung

61
Q

What are the four clinical features of anti-GMB nephritis?

A

Acute kidney failure

Proteinuria

Haematuria

Haemoptysis

62
Q

What is non-proliferative glomerulonephritis?

A

It is characterised by the appearance of a normal glomerulus

63
Q

What are the four subclassifications of non-proliferative glomerulonephritis?

A

Minimal Change Disease

Membranous Glomerulonephritis

Focal Segmental Glomerulosclerosis

Diabetic Nephropathy

64
Q

Is non-proliferative glomerulonephritis nephrotic or nephritic?

A

Nephrotic

65
Q

What is minimal change disease?

A

It is characterised by the presence of minimal damage under a light microscopy

This damage can only be visualised using an electron microscopy – specifically demonstrating shrunken podocytes and effaced foot processes.

66
Q

In which patient group does minimal change disease tend to affect?

A

Children

67
Q

What is a clinical feature of minimal change disease?

A

Oedema

68
Q

What is membranous glomerulonephritis?

A

It is characterised by IgG deposition within between the basal lamina and podocytes within the glomerular basement membrane

This results in a thickened basement membrane, in which new spikes of basal lamina form underneath the podocytes

IgG results in the activation of complement 3 (C3), which attacks the basal lamina thus creating gaps within the basement membrane that albumin can leak through

69
Q

What is the most common classification of glomerulonephritis?

A

Membranous glomerulonephritis

70
Q

What are the causes of membranous glomerulonephritis? Which is most common?

A

Idiopathic - most common

Malignant

Rheumatoid disorders

Drugs (NSAIDs)

71
Q

How do we diagnose membranous glomerulonephritis?

A

We can conduct an immunology screen to look for the presence of anti-phospholipid A2 receptors (PLA2R)

The IgG deposits are not filtered into the urine. An elevated level of IgG is only identified within blood

72
Q

What is focal segmental glomerulosclerosis?

A

It is characterised by scarring of less than 50% of glomerulus tissue

73
Q

What subclassification has a high progression risk into end stage kidney disease?

A

Focal segmental glomerulosclerosis

74
Q

What is diabetic nephropathy?

A

It is characterised by the deposition of glycated molecules in the basal lamina and mesangial matrix

This results in a thickened, leaky glomerular membrane that allows the leakage of albumin and compression of the capillaries supported by the mesangial matrix

75
Q

What are the deposits in diabetic nephropathy called?

A

Kimmelsteil-Wilson lesions

76
Q

How do we screen diabetic patients for diabetic nephropathy?

A

Albumin: creatinine ratio

U&Es

77
Q

What are the four investigations used to diagnose glomerulonephritis?

A

Urine sample

Blood tests

Kidney biopsy

Immunology screen

78
Q

What five urine sample results indicate glomerulonephritis?

A

Haemoglobin, which is elevated

WBCs, which is elevated

Proteinuria, which is an elevated albumin level > 30mg/g

Creatinine, which is elevated > 15900umol over 24hrs

Urea, which is elevated > 20g over 24hrs

79
Q

What seven blood test results indicate glomerulonephritis?

A

Haemoglobin, which is reduced < 130g/L

Serum Creatinine, which is elevated >120 umol/L (80, 160

Serum Urea, which is elevated > 7mmol/L

Serum Albumin, which is reduced < 35g/L

Cholesterol, which is elevated > 5.5mmol/L

eGFR, which is elevated > 120mL/min/1.73m2

Compliment Component C3, which is reduced

80
Q

What is a kidney biopsy?

A

A kidney biopsy involves using a special needle to extract small pieces of kidney tissue for light and electron microscopic examination

81
Q

How are kidney biopsies used to diagnose glomerulonephritis?

A

It enables classification of glomerulonephritis

82
Q

How is an immunology screen used to diagnose glomerulonephritis?

A

It identifies the presence of associated antibodies, such as ANCA antibodies and anti-GMB antibodies.

83
Q

How do we conservatively treat glomerulonephritis?

A

It involves encouraging a low salt diet, as this will improve the patient’s oedema

84
Q

What are the four pharmacological treatments of glomerulonephritis?

A

Hypertensive Agents

Statins

Steroids

Loop Diuretics

85
Q

What two hypertensive agents are used to treat glomerulonephritis?

A

ACEI

ARBs

86
Q

What two statins are used to treat glomerulonephritis?

A

Warfarin

Heparin

87
Q

What three steroids are used to treat glomerulonephritis?

A

Prednisolone

Cyclophosphamide

Azathioprine

88
Q

What are the three complications of glomerulonephritis?

A

Acute Kidney Failure

Chronic Kidney Disease

Hypertension

89
Q

How does glomerulonephritis result in acute kidney failure?

A

This is due to the glomerular damage can result in the rapid accumulation of waste products

90
Q

How does glomerulonephritis result in hypertension?

A

This is due to the fact that damage to the kidneys results in a build-up of waste products in the bloodstream, which can raise blood pressure

Year Two - Urinary System (15 decks)

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