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Glomerulonephritis Flashcards

1
Q

What is glomerulonephritis?

A

Immune-mediated disease of the kidneys affecting the glomeruli

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2
Q

How can glomerulonephritis be classified?

A
  • Aetiology (Primary vs secondary)
  • Histopathology
  • Clinical syndromes
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3
Q

What are some primary syndromes of glomerulonephritis?

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
  • Membrano-proliferative glomerulonephritis
  • IgA nephropathy
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4
Q

What are some secondary causes of glomerulonephritis?

A

Goodpasture’s disease
Circulating immune complexes
Vasculitis

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5
Q

What are some causes of circulating immune complexes causing glomerulonephritis?

A

Infection
Drugs
Cancer - Lymphomas
SLE

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6
Q

What are some forms of infective causes of glomerulonephritis?

A

Hepatitis
Bacteria - Post-streptococcal GN
HIV

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7
Q

How does post-streptococcal GN present?

A

GN symptoms occurring around 2 weeks after streptococcal infection

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8
Q

What are some drugs that can cause glomerulonephritis?

A

Gold
Penicillamine

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9
Q

What are some histological classes of glomerulonephritis?

A

Proliferative vs non-proliferative
Focal vs diffuse
Global vs segmental
Cresentic?

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10
Q

What is meant by proliferative GN?

A

GN with presence of proliferation of mesangial cells

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11
Q

What is meant by non-proliferative GN?

A

GN without presence of proliferation of mesangial cells

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12
Q

What is meant by focal GN?

A

GN in which < 50% of glomeruli are affected

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13
Q

What is meant by diffuse GN?

A

GN in which > 50% of glomeruli are affected

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14
Q

What is meant by global GN?

A

GN in which all of the glomerulus is affected

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15
Q

What is meant by segmental GN?

A

GN in which only part of the glomerulus is affected

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16
Q

What is meant by crescentic GN?

A

GN in which there are crescents:
- Epithelial cell extra-capillary proliferation

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17
Q

What are some clinical syndromes of GN?

A

Nephritic syndrome
Nephrotic syndrome
Rapidly progressive glomerulonephritis
Asymptomatic haematuria or proteinuria

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18
Q

What are some ways in which the humeral immune system can lead to glomerulonephritis

A

Ig’s against normal glomerular constituents
Ig’s against non-self antigens
Deposition of immune complexes
Complement activation and inflammatory mediators

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19
Q

What conditions can cause Ig’s against normal glomerular constituents?

A

Goodpasture’s disease
Membranous nephropathy

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20
Q

What conditions can cause Ig’s against non-self antigens in GN?

A

ANCA
IgA nephropathy

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21
Q

What conditions can cause deposition of circulating immune complexes in GN?

A

Post-infectious GN

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22
Q

What conditions cause complement activation and inflammatory mediator release in GN?

A
  • C3 glomerulopathy
  • Post-infectious glomerulonephritis
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23
Q

What are some conditions that cause cell-mediated immune response in GN, resulting in cytokine and GF release from T-cells and macrophages?

A
  • Focal segmental glomerulosclerosis
  • Crescentic glomerulonephritis
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24
Q

What results from mesangial damage in GN?

A

Inflammation within the mesangium results in proliferation and Ang2 and chemokine release
This causes proliferative lesion formation and attraction of inflammatory cells
This causes endothelial damage and therefore RBC leakage

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25
Q

What results from podocyte damage in GN?

A

Podocyte damage causes podocyte atrophy, casing loss of size/charge specific barrier
This leads to a non-proliferative lesion and protein leakage (Proteinuria)

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26
Q

What is rapidly progressive glomerulonephritis?

A

This is the immune mediated rapid loss of renal function over days, weeks or a few months, presenting with severe nephritic syndrome

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27
Q

What investigations are required in RPGN?

A

Kidney biopsy
Serological testing
Early!

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28
Q

Describe the histology of RPGN

A

Crescent formation on renal biopsy

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29
Q

What are some ANCA +ve causes of RPGN?

A
  • Granulomatosis with polyangiitis (GPA)
  • Microscopic polyangiitis (MPA)
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30
Q

What are some ANCA -ve causes of RPGN?

A
  • Goodpasture’s disease
  • Henoch-Schonlein purpura
  • Systemic lupus erythematosus
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30
Q

What are some important history points in GN history taking?

A
  • Foamy or frothy urine?
  • Rashes/Eye symptoms/Respiratory symptoms
  • Recent infections
  • Family history
  • Medication or drug use
31
Q

What are some possible examinations findings in GN?

A
  • Oedema - Periorbital oedema in the morning
  • Huekrcke lines in nails
  • Xanthelasma
  • Rashes - Petechial or purpuric
  • Synovitis
  • Hypertension
32
Q

What tests are required in GN?

A

Bloods
Urine investigations
Kidney USS
Renal biopsy

33
Q

What bloods are required in GN?

A

U+E (AKI or CKD)
Immunological testing (E.g. ANCA, Anti-GBM)

34
Q

What urine investigations are required in GN?

A

Urinalysis (Haematuria, proteinuria)
Urine microscopy
Urine Protein:Creatinine (PCR) on 24-hour urine

35
Q

What are the 4 main stages of proteinuria?

A

Microalbuminuria (30-300mg/day)
Asymptomatic proteinuria (<1g/day)
Heavy proteinuria (1-3g/day)
Nephrotic syndrome (>3g/day)

36
Q

What may be seen on urine microscopy in GN?

A

Dysmorphic RBCs
RBC casts
Granular casts
Lipiduria

37
Q

What may be seen on kidney USS in GN?

A

Small kidneys
Severe cortical thinning

38
Q

What are the 3 main tests which may be performed on a renal biopsy sample?

A

Light microscopy
Electron microscopy
Immunofluorescence

39
Q

What may be seen on light microscopy in GN?

A

Hypercellularity - Inflammatory and reactive proliferations
Sclerosis
Crescents (In RPGN)
Granulomas (In GPA and Sarcoid)

40
Q

What may be seen on electron microscopy in GN?

A

Immune complex depositions in the basement membran e

41
Q

What may be shown on immunofluorescence in GN?

A

Antibody type and distribution

42
Q

What will be seen on immunofluorescence in Goodpasture’s GN?

A

Linear IgG in basement membrane

43
Q

What are the aims of treatment in GN?

A

Reduce proteinuria, induce remission of nephrotic syndrome and preserve long-term renal function

44
Q

What is meant by complete remission of nephrotic syndrome?

A

Proteinuria < 300mg/day

45
Q

What is meant by partial remission of nephrotic syndrome?

A

Proteinuria < 3-3.5g/day

46
Q

What are some non-immunosuppressive management options for GN?

A
  • Anti-hypertensives (ACEi/ARB)
  • Diuretics
  • Statins
  • Anticoagulation (Nephrotic syndrome with hypoalbuminaemia)
  • Salt and fluid restriction (Nephrotic syndrome)
47
Q

What are some immunosuppressive drugs used to manage GN?

A

Corticosteroids
Alkylating agents
Calcineurin inhibitors
Anti-proliferative

48
Q

What are some examples of alkylating agents?

A

Cyclophosphamide
Chlorambucil

49
Q

What are some examples of calcineurin inhibitors?

A

Cyclosporin
Tacrolimus

50
Q

What are some examples of anti-proliferative drugs?

A

Azathioprine
Mycophenolate Mofentil

51
Q

What are some forms of immunosuppressive treatments of GN?

A

Drugs
Pasmapharesis
Antibodies (IV Ig)

52
Q

Management of RPGN

A

Strong immunosuppressives
Dialysis

53
Q

What is the most common form of GN in children?

A

Minimal change disease

54
Q

What is the possible pathology of minimal change disease?

A

Unknown cause, however, there is thought to be some involvement of B-cells and anti-nephron antibodies

55
Q

Histology of minimal change disease

A

Characteristic diffuse effacement of the podocyte foot processes on electron microscopy

Normal on LM and IF

56
Q

Treatment of minimal change disease

A
  • 1st line - Oral corticosteroids
  • 2nd line - Cyclophosphamide/Rituximab
57
Q

What is focal segmental glomerulosclerosis?

A

This is a histological lesion rather than a disease and is the 2nd most common cause for nephrotic syndrome in adults

58
Q

Primary cause of focal segmental glomerulosclerosis

A

General podocyte dysfunction

59
Q

Secondary causes of focal segmental glomerulosclerosis

A
  • HIV
  • Drugs - pamidronate, interferon, heroin and obesity
60
Q

Histology of focal segmental glomerulosclerosis

A

Sclerosis in parts of some glomeruli on LM
No immune deposits or foot process effacement

61
Q

Treatment of focal segmental glomerulosclerosis

A
  • 1st line - High dose glucocorticosteroids
  • 2nd line - CNIs - Calcineurin inhibitors (E.g. tacrolimus)
62
Q

Prognosis of focal segmental glomerulosclerosis

A

50% will progress to ESRF after 10 years

63
Q

What is membranous nephropathy

A

This is another pattern of injury found on histology, instead of a disease and is the commonest cause of nephrotic syndrome in adults

64
Q

Primary cause of membranous nephropathy

A

Anti-PLA2R antibodies

65
Q

Secondary causes of membranous nephropathy

A
  • Infection - HepB, Parasites
  • Connective tissue disease - Lupus
  • Malignancy - Carcinomas, Lymphomas
  • Drugs - Gold, Penicillamine
66
Q

Histology of membranous nephropathy

A
  • Thickening of GBM on LM
  • Spike and dome pattern with silver staining on LM
  • Subepithelial immune complex deposition in the GBM on EM
67
Q

Treatment of membranous nephropathy

A

immunosuppression - Cyclophosphamide

68
Q

What is membranoproliferative GN

A

MPGN is a histologic lesion and not a specific disease entity

It’s pattern of injury once identified will require further evaluation to find underlying causes.

69
Q

What are the 2 primary mechanisms of MPGN?

A
  • Immune complex deposition and activation of complement
  • Complement dysregulation leading to persistent activation of alternative pathway
70
Q

Histology of MPGN

A
  • Thick capillary wall
  • Glomerular membrane proliferation
  • Immunofluorescent microscopy shows immune complex deposition in capillary walls
71
Q

Treatment of MPGN

A
  • Treating underlying infections etc (Hep C)
  • Immunosuppression with steroids/ MMF for idiopathic cases
  • Complement inhibitors such as eculizumab for disregulation
72
Q

What is the most common form of GN in adults in the world?

A

IgA nephropathy (Berger’s disease)

73
Q

How will IgA nephropathy usually present?

A
  • 10-20 years old
  • Asymptomatic microhaematuria ± Non-nephrotic range proteinuria
  • Macroscopic haematuria post-infection
  • AKI/CKD
74
Q

What causes IgA nephropathy?

A

This can be caused by respiratory or GI infection and there is an association with Henoch-Schönlein purpura

75
Q

Histology of IgA nephropathy

A
  • Mesangial cell proliferation and expansion on light microscopy
  • IgA deposits in mesangium on immunofluorescence
76
Q

Treatment of IgA nephropathy

A
  • SGLT2 inhibitors
  • Budesonide
  • Dual endothelin-angiotensin receptor antagonist (Sparsentan)

Renal (41 decks)

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