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Paediatric renal/urinary > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What is glomerulonephritis?

A

Damage to the glomerulus including glomerular basement membrane and glomerular capillaries, usually caused by inflammatory change

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2
Q

What are the types of glomerulonephritis?

A
  1. Membranous glomerulonephritis
  2. Minimal change disease
  3. Focal segmental glomerulonephritis
  4. IgA nephropathy
  5. Rapidly progressing glomerylonephritis
  6. Lupus nephritis
  7. Post-infectious glomerunephritis
  8. Anti-glomerular basement membrane antibody (anti-GBM) disease
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3
Q

What are the causes of glomerulonephritis?

A 
1. Infections e.g. 
=> group A 
=> streptococcus, 
=> hepatitis B and C, 
=> respiratory & gastrointestinal tract infections, 
=> endocarditis, 
=> HIV
  1. Systemic inflammatory conditions e.g.
    => lupus,
    => rheumatoid
    => arthritis,
    => anti-glomerular basement membrane disease,
    => microscopic polyangiitis,
    => granulomatosis polyangiitis
  2. Drugs e.g. NSAID, gold, anabolic steroids
  3. Metabolic disorders e.g. diabetes, hypertension and thyroid disease
  4. Malignancy
  5. Hereditary disorders e.g. Alpert’s syndrome
  6. Deposition diseases e.g amyloidosis
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4
Q

What are the signs and symptoms of glomerulonephritis?

A

May be asymptomatic

=> Haematuria (macro or microscopic)

=> Proteinuria

=> Oedema

=> Hypertension

=> Joint pain

=> Rash

=> Fever

=> Weight loss

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5
Q

What are the investigations for glomerulonephritis?

A
  1. Urinalysis
    => may show haematuria, proteinuria
  2. Urine microscopy
  3. U&E
    => may show reduced GFR or elevated creatinine
  4. FBC
    => may show anaemia or inflammatory response
  5. Metabolic profile
    => may show underlying diabetes
  6. Lipid profile
    => may show hyperlipidaemia
  7. C-reactive protein
  8. Testing for specific systemic causes e.g. ESR, rheumatoid factor, anti-GBM antibodies
  9. Renal tract ultrasound
    => assess kidney size and evidence of obstruction
  10. Renal biopsy
    => definitive test for diagnosis of glomerulonephritis
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6
Q

How do you treat glomerulonephritis?

A
  1. Antibiotics if infection
  2. ACEi to decrease proteinuria
  3. Corticosteroids
  4. Furosemide if hypertension and fluid overload
  5. Immunosuppressant drugs
  6. Plasmapheresis
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7
Q

How does acute glomerulonephritis present:

i) uncomplicated
ii) complicated

A 
i) Uncomplicated:
=> Haematuria 
=> Oliguria 
=> Raised BP (50%)
=> Peri-orbital oedema
=> Fever
=> GI disturbance
=> Loin pain

ii) Complicated:

1. Hypertensive encephalopathy: 
=> Restless
=> Drowsy
=> Severe headaches
=> Fits
=> Reduced vision
=> Vomiting
=> Coma 
2. Uraemia:
=> Acidosis
=> Twitching
=> Stupor
=> Coma
  1. Cardiac:
    => Gallop rhythm
    => Cardiac failure ± enlargement
    => Pulmonary oedema

*produced by an immune glomerulonephritis in the kidneys

**Peak age 7 years

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8
Q

What investigations are carried out for acute glomerulonephritis?

A
  1. Blood test:
    => FBC, U&E (creatinine, potassium, bicarbonate, calcium, phosphate and albumin)

=> Complement (low C3, normal C4)

=> Antinuclear factors (ANA);
=> Anti-DNA antibodies (if SLE suspected);
=> Anti-neutrophil cytoplasmic antibodies (ANCA) if vasculitis suspected

=> Syphillis serology, blood cultures, virology

  1. Mid stream urine (MSU)
    => check urine culture & specific gravity
  2. Throat swab
  3. Urgent renal ultrasound / CXR if fluid overload suspected

5.

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9
Q

What is post streptococcal glomerulonephritis (PSGN)?

A

PSGN is a type of glomerular nephritis that occurs 7-14 days after a steptococcal throat or skin infection (pharyngitis or impetigo)

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10
Q

What are the causes of post-streptococcal glomerulonephritis?

A
  1. Group A beta-haemolytic streptococci (Strep pyogenes)

=> Immune complex deposition (IgG, IgM, C3) in the glomeruli, neutrophil infiltration and complement activation in the glomerulus causing inflammation and/or proliferation

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11
Q

What are the clinical features of post-streptococcal glomerulonephritis?

A
  1. Sudden onset of gross haematuria (cola-coloured urine)
  2. Oliguria/proteinuria => periorbital oedema (due to salt retention in the loose skin)
  3. Headache / malaise / anorexia
  4. Hypertension
  5. Fever
  6. Abdominal pain
  7. Bloods: Low C3 & raised ASO titre

=> Typical nephrite syndrome presentation

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12
Q

What are the differentials for post-streptococcal glomerulonephritis?

A

SHARP AIM

=> SLE
=> Henoch-Schönlein purpura
=> Anti glomerular basement membrane (GBM) disease (aka goodpasture's disease)
=> Rapidly progressive glomerulonephritis 
=> Post-streptococcal GN
=> Alport's syndrome 
=> IgA nephropathy 
=> Membranoproliferative GN
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13
Q

What are the investigations carried out for post-streptococcal glomerulonephritis?

A
  1. First line investigation: urinalysis and microscopy, culture and sensitivities (MC&S)

=> Urinalysis is positive for protein, blood or both.
=> Urine MC&S: presence of red blood cells (normally dysmorphic, which suggests bleeding from glomerulus), white blood cells (neutrophil infiltration is one of the mechanisms of damage in nephritic syndrome) and associated casts.

  1. Blood tests:
    => FBC for raised white cells, suggestive of an infective process,
    => U&Es for signs of acute kidney injury (raised urea & creatinine)
    => Immunoglobulins, complement (low C3 levels)
    => Autoantibodies i.e raised anti-streptolysin titre (confirms recent strep infection), raised DNAse B titre = an autoimmune process.
  2. Blood cultures indicated in patients with fever.

Imaging is rarely helpful.

*The GOLD standard method for diagnosis is RENAL BIOPSY => typically not needed.

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14
Q

Post-streptococcal glomerulonephritis is managed conservatively.

=> Sodium restrictions
=> Diuretics
=> Anti-hypertensives
=> Restrict protein in oliguric phase
=> Give penicillin orally for 10 days
=> Check BP often

*Oedema lasts 5-10 days but HTN, haematuria, proteinuria may last for several weeks

A

Complications include:

Chronic kidney disease

End stage renal disease

*but carries a good prognosis.

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15
Q

What features are seen in renal biopsy?

A
  1. Post-streptococcal glomerulonephritis causes acute, diffuse proliferative glomerulonephritis
  2. Endothelial proliferation with neutrophils
  3. Electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
  4. Immunofluorescence: granular or ‘starry sky’ appearance
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16
Q

What is IgA nephropathy?

A

IgA nephropathy aka Berger’s disease is the commonest cause of glomerulonephritis world wide.

=> develops 1-2 days after URTI.

Assoc. with
=> alcoholic cirrhosis
=> coeliac disease / dermatitis herpetiformis
=> Henoch-Schonlein purpura

17
Q

How does IgA nephropathy present?

A

Classically presents as recurrent macroscopic haematuria, typically in young male following an upper respiratory tract infection.

=> nephrotic range proteinuria is rare

=> renal failure is unusual

18
Q

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis:

  1. Post-streptococcal glomerulonephritis is associated with low complement levels
  2. Main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
  3. There is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis
19
Q

How is IgA nephropathy managed?

A
  1. Isolated haematuria, no or minimal proteinuria and a normal glomerular filtration rate (GFR) =>
    no treatment needed; follow-up to check renal function
  2. Persistent proteinuria, a normal or only slightly reduced GFR =>
    initial treatment with ACE inhibitors
  3. If there is active disease (e.g. falling GFR) or failure to respond to ACE inhibitors
    immunosuppression with corticosteroids
20
Q

What is the prognosis for IgA nephropathy?

A
  1. 25% of patients develop ESRF
  2. Markers of good prognosis: frank haematuria
    markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD
21
Q

What is Alport’s syndrome?

A

Inherited in an X-linked dominant pattern
=> due to a defect in the gene coding for type IV collagen
=> results in an abnormal glomerular-basement membrane (GBM)

*disease is more severe in males, with females rarely developing renal failure

22
Q

What are the features of Alport’s syndrome?

A

=> microscopic haematuria

=> progressive renal failure

=> bilateral sensorineural deafness

=> lenticonus: protrusion of the lens surface into the anterior chamber

=> retinitis pigmentosa

=> renal biopsy: splitting of lamina densa seen on electron microscopy

23
Q

How is Alport syndrome diagnosed?

A
  1. Molecular genetic testing
  2. Renal biopsy
    electron microscopy: characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance

Paediatric renal/urinary (8 decks)

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