Clinical Glomerular Disease Flashcards

1
Q

What is glomerulonephritis?

A
  • A group of inflammatory disorders of the disease and are responsible for almost 30% of ESRD.
  • They are classified based on morphology and the majority are attributed to autoimmune aetiologies
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2
Q

What are the features of glomerulonephritis?

A
  • Haematuria
  • Proteinuria
  • Hypertension
  • Renal insufficiency
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3
Q

How does macroscopic haematuria present?

A

Tea or cola coloured or frank blood

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4
Q

How does microscopic haematuria present?

A

> 5 RBC per high power field

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5
Q

In what syndrome does haematuria present more often?

A

Nephritic> nephrotic

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6
Q

What can the source of haematuria be?

A
  • Kidneys
  • Ureters
  • Bladder
  • Prostate
  • Urethra
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7
Q

How does haematuria present in glomerulonephritis?

A

Persistent microscopic haematuria. Microscopy shows dysmorphic RBC (Mickey mouse like)

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8
Q

How does proteinuria present in glomerulonephritis?

A

Persistent, proteinuria of more than 1 gram /mmol creatinine.

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9
Q

How can proteinuria be investigated?

A

Urine protein creatinine ratio or 24 hour urine collection

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10
Q

What is considered hypertension?

A

> 140/80mmHg

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11
Q

Does proteinuria occur more in nephrotic or nephritic syndrome?

A

Equal

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12
Q

Does hypertension occur more in nephrotic or nephritic syndrome?

A

Nephritic> nephrotic

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13
Q

What are the features of nephritic syndrome?

A
  • Active urine sediment: haematuria, dysmorphic RBCs and cellular casts
  • Hypertension
  • Renal impairment
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14
Q

What are the features of nephrotic syndrome?

A
  • Oedema
  • Proteinuria >3.5 g/day
  • Hypoalbuminemia
  • Hyperlipidemia
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15
Q

What can cause nephrotic syndrome?

A

Primary (idiopathic) glomerular disease or secondary glomerular disease

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16
Q

What is the differential diagnosis for nephrotic syndrome?

A
  • Congestive heart failure (JVP raised, normal albumin, minimal proteinuria)
  • Hepatic disease (abnormal LFTs, no proteinuria)
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17
Q

What can glomerulonephritis be classified according to?

A
  • Aetiology
  • Primary vs secondary (kidneys alone or multisystem disease)
  • Morphological
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18
Q

What is the aetiology of glomerulonephritis?

A
  • Autoimmune
  • Infection
  • Malignancy
  • Drugs
  • Others
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19
Q

What is proliferative glomerulonephritis?

A

Excessive numbers of cells in glomeruli. These include infiltrating leucocytes

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20
Q

What is non-proliferative glomerulonephritis?

A

Glomeruli look normal or have areas of scarring. They have normal numbers of cells

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21
Q

Define diffuse glomerulonephritis.

A

> 50% of glomeruli affected

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22
Q

Define focal glomerulonephritis.

A

<50% of glomeruli affected

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23
Q

Define global glomerulonephritis.

A

All the glomerulus affected

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24
Q

Define segmental glomerulonephritis

A

Part of the glomerulonephritis

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25
Q

What glomerulonephritis presents with urinary sediment abnormalities?

A

IgA nephropathy

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26
Q

What glomerulonephritis presents with proteinuria?

A

IgA nephropathy

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27
Q

What types of glomerulonephritis present with nephrotic syndrome?

A
  • Minimal change disease

- Membranous nephropathy

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28
Q

What types of glomerulonephritis present with nephritis state?

A
  • Anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis
  • Post infection glomerulonephritis
29
Q

Give 4 examples of proliferative glomerulonephritis?

A
  • Post infective nephritis
  • Mesangial IgA disease
  • Focal necrotising (crescentic) nephritis
  • Membrano-proliferative nephritiis
30
Q

What does post-streptococcal glomerulonephritis usually follow?

A

Follows 10-21 days after infection typically of throat or skin.

31
Q

What bacteria is post-streptococcal glomerulonephritis most commonly associated with?

A

Lancefield group A streptococci

32
Q

What genetic predisposition is associated with post-streptococcal glomerulonephritis?

A

HLA-DR, -DP, -DP

33
Q

What is the treatment for post-infective glomerulonephritis?

A
  • Antibiotics for infection, debatable.
  • Loop diuretics such as frusemide for oedema
  • Vasodilator drugs (e.g. amlodipine) for hypertension
34
Q

What is the commonest cause of glomerulonephritis?

A

IgA nephropathy

35
Q

What is IgA nephropathy characterised by?

A

Characterized by IgA deposition in the mesangium +mesangial proliferation.

36
Q

Who is most commonly affected by IgA nephropathy?

A

Most common in 2nd and 3rd decade of life with males more commonly affected.

37
Q

What is the prognosis of u[ to 40% of those with IgA nephropathy?

A

Progress to ESRD

38
Q

How does IgA nephropathy present?

A
  • Microscopic haematuria.
  • Microscopic haematuria + proteinuria
  • Nephrotic syndrome
  • IgA crescentic glomerulonephritis
39
Q

What are the causes of crescentic glomerulonephritis?

A
  • Anti-neutrophil cytoplasmic antibody (ANCA)-associated
  • Anti-glomerular basement membrane (GBM)
  • IgA vasculitis
  • Post infection glomerulonephritis
  • SLE
40
Q

What ANCA associated glomerulonephritis is there?

A
  • Microscopic polyangiitis
  • Granulomatosis with polyangiitis
  • Eosinophilic granulomatosis with polyangiitis
41
Q

What anti-glomerular basement membrane glomerulonephritis is there?

A
  • Anti-GBM nephritis

- Goodpasture’s syndrome

42
Q

What is anti-GBM disease?

A

A rare disease caused by circulating GBM

43
Q

What can anti-GBM disease present as?

A
  • Nephritis (anti-GBM glomerulonephritis)

- Nephritis+ lung haemorrhage (Goodpasture’s syndrome)

44
Q

What are the 2 peaks in life for anti-GBM disease?

A
  • 3rd decade

- 6th/7th decade

45
Q

How is anti-GBM disease diagnosed?

A

Diagnosed by demonstrating anti-GBM antibodies in serum and kidney

46
Q

How is anti-GBM disease treated?

A
  • Aggressive immunosuppression
  • Steroids
  • Plasma exchange
  • Cyclophosphamide
47
Q

What is the management for crescentic glomerulonephritis?

A
  • Immunosuppression
  • Corticosteroids
  • Plasma exchange
  • Cytotoxic e.g. Cyclophosphamide
  • B-cell therapy e.g. Rituximab
  • Complement inhibitors
48
Q

What is the prognosis for crescentic glomerulonephritis?

A

Good provided treatment is started early enough

49
Q

What syndrome do proliferative glomerulonephritides present with?

A

Nephritic

50
Q

Give 3 examples of non-proliferative glomerulonephritis

A
  • Minimal Change Disease
  • Focal and segmental glomerulonephritis
  • Membranous Nephropathy
51
Q

What are the general measures in the treatment of nephrotic syndrome?

A
  • Treat oedema: salt and fluid restriction and loop diuretics.
  • Hypertension: use Renin-Angiotensin-Aldosterone-blockade.
  • Reduce risk of thrombosis: Heparin or Warfarin.
  • Reduce risk of infection e.g. pneumococcal vaccine.
  • Treat dyslipidemia e.g. statins.
52
Q

What is the commonest form of glomerulonephritis in children?

A

Minimal change nephrotic syndrome

53
Q

How does minimal change disease usually present?

A
  • Sudden onset of oedema

- Complete loss of proteinuria with steroids

54
Q

What is the initial treatment for minimal change disease?

A
  • Prednisolone – 1mg/kg for up to 16 weeks.
  • Once remission achieved , slow taper over 6 months.
  • Initial relapse treated with further steroid course.
55
Q

How are subsequent relapses of minimal change disease treated?

A
  • Cyclophosphamide
  • Cyclosporin
  • Tacrolimus
  • Mycophenolate mofetil
  • Rituximab
56
Q

What is the prognosis of minimal change disease?

A
  • Despite relapsing behaviour, prognosis is favourable.
  • Risk of end stage kidney disease is low.
  • Steroids toxicity as multiple exposure.
57
Q

What are the general measures for the management of minimal change disease?

A
  • Salt and fluid restrictions.
  • Daily weights.
  • Loop diuretic e.g. Furosemide.
  • Thromboprophylaxis e.g. low molecular weight heparin.
58
Q

What does focal and segmental glomerulonephritis present with?

A

Nephrotic syndrome

59
Q

What does pathology of focal and segmental glomerulonephritis reveal?

A

Focal and segmental sclerosis with distinctive patterns e.g. tip lesion, collapsing, cellular, perihilar, and not otherwise specified..

60
Q

What are focal and segmental glomerulonephritis generally resistant to?

A

Steroids

61
Q

What is there a high chance of progression to in focal and segmental glomerulonephritis?

A

ESRD

62
Q

How is focal and segmental glomerulonephritis treated?

A
  • General measures
  • Trial of steroids, positive response , even partial remission, carries better prognosis.
  • Alternative options: cyclosporin, cyclophosphamide, and Rituximab.
63
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy

64
Q

What is the cause of the majority of membranous nephropathy cases?

A

Idiopathic

65
Q

What are the serological markers for membranous nephropathy?

A
  • Anti-phospholipase A2 receptor (PLA2R) antibody positive in 70% of idiopathic cases
  • Thrombospondin type 1 domain containing 7A (THSD7A).
66
Q

What are secondary causes of membranous nephropathy?

A
  • Malignancies
  • SLE
  • Rheumatoid arthritis.
  • Drugs: NSAIDs, gold, penicillamine.
67
Q

What is the treatment for membranous nephropathy?

A
  • General measures for at least 6 months.
  • Immunosuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function.
  • Cyclophosphamide and steroids (alternate months) for 6 months.
  • Cyclosporine.
  • Rituximab.
68
Q

What is the prognosis of membranous nephropathy?

A
  • Resolves spontaneously in a third.
  • Prognosis good in treated patients whose proteinuria resolves
  • About 25% are on dialysis at 10 years
  • Can recur in renal transplants
69
Q

What is the key investigation for glomerulonephritis?

A

Renal biopsy