Glomerulonephritis Flashcards

1
Q

What conditions does the term ‘glomerulonephritis’ encompass?

A
  • Caused by pathology in the glomerulus
  • Present with proteinuria, haematuria, or both
  • Are diagnosed on a renal biopsy
  • Cause CKD
  • Can progress to kidney failure
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2
Q

The glomerulonephritides classically present on a spectrum ranging from nephrosis to nephritis. What’s the difference?

A
  • Nephrosisproteinuria due to podocyte pathology
  • Nephritishaematuria due to inflammatory damage
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3
Q

Which investigations are done for glomerulonephritis?

A
  • Urine → dipstick / MC+S / Bence-Jones protein
  • Vitals → may be hypertensive
  • Bloods → FBC / U+Es / LFT / CRP / Igs / Electrophoresis / Complement / Autoantibodies
  • CXR → pulmonary haemorrhage
  • Renal USS → size and anatomy for biopsy
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4
Q

What is IgA nephropathy?

A
  • Commonest primary GN in high-income countries
  • Typically young adult with haematuria following an URTI
  • Can be asympatomatic with non-visible haematuria
  • May be hypertensive
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5
Q

How is IgA nephropathy diagnosed?

A

Renal biopsy → IgA deposition in mesangium

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6
Q

What is the treatment for IgA nephropathy?

A
  • ACE-i / ARB reduce proteinuria and protect renal function
  • Corticosteroids if persistent proteinuria >1g despite 3-6months of ACE-i/ARB and GFR > 50
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7
Q

What are clinical features of HSP?

A
  • Seen following infection
  • Palpable purpuric rash (w/ localised oedema) over buttocks and extensors
  • Abdo pain
  • Polyarthritis
  • Features of IgA nephropathy may occur (haematuria, renal failure)
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8
Q

What is the treatment for HSP?

A
  • Analgesia for arthralgia
  • Treatment of nephropathy generally supportive
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9
Q

What are features of post-streptococcal GN?

A
  • Occurs after a throat (2ks) or skin (3-6wks) infection
  • Streptococcal antigen deposits in the glomerulus leading to immune complex formation and inflammation
  • Young children most commonly infected
  • Presentation varies from haematuria to acute nephritis (haematuria, oedema, HTN)
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10
Q

How is post-strep GN diagnosed?

A
  • Increased ASO titre (Antistreptolysin O antibodies)
  • Increased Anti-DNAse B
  • Reduced C3
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11
Q

How do you differentiate between IgA nephropathy and post-strep glomerulonephritis?

A
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12
Q

What is the treatment for post-strep GN?

A

Supportive abx to clear nephritogenic bacteria

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13
Q

What is anti-glomerular basement membrane (Anti-GMB) disease?

A
  • Prev known as Goodpasture’s disease
  • Rare
  • Auto-antibodies to type IV collagen present in glomerular and alveolar basement membranes
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14
Q

What is the clinical presentation of Anti-GBM disease?

A
  • Renal → oliguria / haematuria / AKI / renal failure
  • Lung → pulm haemorrhage / SoB / haemoptysis
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15
Q

What is the treatment for Anti-GBM disease?

A
  • Plasma exchange
  • Corticosteroids
  • Cyclophosphamide
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16
Q

Rapidly progressive glomerulonephritis is any agressive GN, rapidly progressing to renal failure over days or weeks.

What are causes of rapidly progressive GN?

A
  • Small vessel/ANCA vascuilitis
  • Lupus nephritis
  • Anti GBM disease
17
Q

How is rapidly progressive GN diagnosed?

A

Breaks in GBM allow an influx of inflammatory cells so that crescents are seen on renal biopsy

18
Q

What is the treatment for rapidly progressive GN?

A
  • Corticosteroids
  • Cyclophosphamide