Glomerulonephritis Flashcards

1
Q

Define glomerulonephritis?

A

Conditions causing inflammation of or around the glomerulus.

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2
Q

What is nephritic syndrome?

List 5 features

A

Heamaturia due to inflammatory damage.

  1. Haematuria
  2. Oliguria
  3. Proteinuria (less than 3g/24hr)
  4. Fluid retention.
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3
Q

What is nephrotic syndrome?

List 4 features

A

Proteinuria due to podocyte damage.

  1. Proteinuria >3g/24hr
  2. Hypoalbuminaemia <30g/L
  3. Peripheral oedema
  4. Hyperlipidaemia.
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4
Q
Initial Ix for glomerulonephritis: 
 Bloods (8)
 Urine (3)
 Imaging (2)
 Renal biopsy.
A

Bloods: FBC, U+E, LFT, CRP, immunoglobulins, electrophoresis, complement, autoantibodies (Anti-dsDNA, anti-GBM, ANA, ANCA).
Urine: MC+S, bence jones proteins, A: Cr.
Imaging; CXR, Renal USS

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5
Q

List conditions causing nephritis syndrome (5)

A
  1. IgA nephropathy
  2. Henoch-Schonlein purpura.
  3. Post-streptococcal glomerulonephritis.
  4. Anti-GBM disease.
  5. Rapidly progressive glomerulonephritis.
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6
Q
What is IgA nephropathy (Berger disease)?
and pathophysiology (2 points)
A

Only affects KIDNEYS.
Kidney disease caused by IgA antibody deposition in the kidneys leading to local inflammation.

Galactose deficient IgA is not recognised by the body, thus it accumulates in the kidneys (instead of being degraded).
As it is not recognised as self, anti-glycan antibodies are made. These form immune complexes + are deposited in the mesangium causing inflammation

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7
Q
Features of IgA nephropathy: 
  clinical symptoms (3)
  Ix (1)
  Tx (2)
  Prognosis
A

Clinical features: Asymptomatic. Heamaturia. HTN
Ix: Renal biopsy = IgA deposition in mesangium.
Tx: ACEi (reduced proteinuria). Steroids (Prevent immune complexes)
Prognosis: Slow indolent disease, progresses to renal failure over 30yrs (20-50%)

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8
Q

what is Henoch Schonlein purpura?

A

Small vessel vasculitis = IgA directly attacks small blood vessels.
Systemic variant of IgA nephropathy with IgA deposition in skin, joints, gut, + kidney.

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9
Q

List clinical features of HSP? (4)

A

Palpable purpuric rash on extensor surfaces
Flitting polyarthritis
Abdominal pain (gut bleeding)
Nephritic syndrome

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10
Q

Diagnosis + Tx of HSP?

A

Ix: clinical, renal biopsy = IgA deposition in mesangium.
Tx: ACEi and steroids.

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11
Q

What is post-streptococcal glomerulonephritis?

A

Occurs 3 wks after throat or skin infection.
Streptococcal antigen becomes deposited in the glomerulus + forms immune complexes causing inflammation (type 3 hypersensitivity reaction).

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12
Q

Clinical features of post-step GN? (think nephritis features)

A

Heamaturia
oedema
oliguria
HTN

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13
Q

Ix and Tx of post-strep GN?

A

Ix: High anti-DNAse. low C3.
Tx: supportive.

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14
Q

What is anti-glomerular basement membrane disease:

A

Autoantibodies develop to type 4 collagen, which is found in the glomerular + alveolar basement membrane. These activate complement system.

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15
Q

Anti-GBM disease:
Clinical features (4)
Ix (1)
Tx (2)

A

Clinical features; Heamaturia, AKI, Heamoptysis, sob.
Ix: anti-GBM antibodies
Tx: Plasma exchange. Steroids.

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16
Q

what is rapidly progressive glomerulonephritis?

A

Any glomerulonephritis that progresses to renal failure over days to weeks

17
Q

Causes of rapidly progressive GN? (5)

A
Small vessel vasculitis 
Lupus nephritis 
Anti-GBM disease 
IgA nephropathy 
Membranous glomerulonephritis
18
Q

what is seen on renal biopsy of rapidly progressive GN?

A

Crescent shaped cell proliferation in bowman’s space.

19
Q

Primary causes of nephrotic syndrome? (4)

A

Minimal change disease.
Membranous neuropathy.
Focal segmental glomerulosclerosis. Membranoproliferative GN (MPGN).

20
Q

Secondary causes of nephrotic syndrome? (4)

A

Diabetes
Lupus nephritis
Myeloma
Pre-eclampsia

21
Q

Treatment of nephrotic syndrome? (3)

A
  1. Reduce oedema = Fluid + salt restriction. Furosemide. Daily weight (0.5-1kg loss/day)
  2. Treat cause = Renal biopsy. Steroids.
  3. Reduce proteinuria = ACEi
22
Q

Complications of nephrotic syndrome? (4)

A
  1. Thromboembolism - blood is hypercoagulable.
  2. Infection
  3. Hyperlipidaemia
  4. HTN
23
Q

Minimal change disease:

A

Commonest cause in children.
Cause – idiopathic, drugs, paraneoplastic.
Ix: Normal, electron microscopy = effacement of podocyte foot processes.
Tx: Prednisolone.

24
Q

Focal segmental glomerulosclerosis:

A

Commonest cause in adults.
Cause: Idiopathic. Sickle cell, HIV, heroin.
Biopsy: scarring in some areas of glomerulus.
Tx: ACEi + BP control. 1st steroids. 2nd calcineurin inhibitors.

25
Q

Membranous nephropathy

A

Inflamed glomerular basement membrane.
Cause: Idiopathic. Malignancy, infection, autoimmune. Ix: anti-phospholipid A2 receptor antibody. Thickened GBM.
Tx: ACEi + BP control, steroid (some cases).

26
Q

Membranoproliferative glomerulonephritis

A

Immune deposits in sub-endothelial layer.
Light microscopy - Tram track appearance.
Tx: ACEi + BP control.