Glomerulonephritis

Question 1

What is the treatment for Anti-GBM disease?

Answer 1

• Plasma exchange
• Corticosteroids
• Cyclophosphamide

Question 2

What is the treatment for rapidly progressive GN?

Answer 2

• Corticosteroids
• Cyclophosphamide

Question 3

What is the treatment for HSP?

Answer 3

• Analgesia for arthralgia
• Treatment of nephropathy generally supportive

Question 4

What are clinical features of HSP?

Answer 4

• 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)

Question 5

What are features of post-streptococcal GN?

Answer 5

• 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)

Question 6

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

Answer 6

• Nephrosis → proteinuria due to podocyte pathology
• Nephritis → haematuria due to inflammatory damage

Question 7

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

What are causes of rapidly progressive GN?

Answer 7

• Small vessel/ANCA vascuilitis
• Lupus nephritis
• Anti GBM disease

Question 8

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

Answer 8

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

Question 9

How is rapidly progressive GN diagnosed?

Answer 9

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

Question 10

What is the treatment for IgA nephropathy?

Answer 10

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

Question 11

What is IgA nephropathy?

Answer 11

• 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

Question 12

What is the treatment for post-strep GN?

Answer 12

Supportive abx to clear nephritogenic bacteria

Question 13

How is IgA nephropathy diagnosed?

Answer 13

Renal biopsy → IgA deposition in mesangium

Question 14

What conditions does the term ‘glomerulonephritis’ encompass?

Answer 14

• 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

Question 15

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

Answer 15

Question 16

How is post-strep GN diagnosed?

Answer 16

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

Question 17

Which investigations are done for glomerulonephritis?

Answer 17

• 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

Question 18

What is the clinical presentation of Anti-GBM disease?

Answer 18

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