Lecture 10 Glomerulus Disease (Pathology) Flashcards

1
Q

Name the structures found in the renal corpuscle

A
Afferent arteriole
Podycytes
Mesangial cells
Bowman's capsule
Efferent arteriole
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2
Q

Define Glomerulonephritis

A

Disease of the glomerulus. Can be inflammatory or non-inflammatory

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3
Q

What are the 4 common presentations in Glomerulonephritis

A
  1. Haematuria (blood in urine)
  2. Heavy proteinuria (nephrotic syndrome)
  3. Slowly increasing proteinuria
  4. Acute renal failure
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4
Q

A 40 year old male has discoloured urine which tests positive for blood what investigations should be done

A

Urine culture
Ultrasound
Clotting
Renal biopsy (light microscopy and immunofluorescence)

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5
Q

What are the main causes of haematuria

A

UTI
Urinary tract stone
Urinary tract tumour
Glomerulonephritis

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6
Q

If a patient has IgA Glomerulonephritis what would you see in the renal biopsy with immunofluorescence

A

Immunoglobulin (of IgA type) and complement component C3 in mesangial area of all glomeruli. Causes increased proliferation of mesangial cells

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7
Q

What is the prognosis of IGA Glomerulonephritis

A
  • Usually self-limiting

* Small percentage go onto chronic renal failure (via continued deposition of matrix)

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8
Q

50 year old male
• 3 weeks of feeling unwell and swollen legs
• Send of blood biochemistry and haematology tests  Serum albumin is low
• Dipstick proteinuria
Sliver stain shows spikes surrounds a deposit of Ig
What is the clinical diagnosis

A

Membranous glomerulonephritis

thickened glomerular basement membrane and deposits of IgG seen on electron microscopy

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9
Q

In membranous glomerulonephritis where does the IgG deposit deposit itself

A

Between basal lamina and podocyte

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10
Q

In membranous glomerulonephritis the IgG deposits lead to__

A

activation of C3 which punches holes in the filter. Leaky filter now allows albumin to be filtered into urine

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11
Q

What is the prognosis for membranous glomerulonephritis

A

1/4 will have chronic renal failure in 10 years

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12
Q

What is the underlying cause of of IgG Production and Accumulation in Membranous Glomerulonephritis

A

• In many patients antigen is phospholipase A2 receptor on podocytes

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13
Q

• 31 year old woman
• Type 1 diabetes since 7 years of age
• Long periods of poor glycaemic control
• Developed retinopathy
• Albumin in urine slowly increasing over last few years. Now has heavy protein leakage into urine
• Check clotting screen then do renal biopsy
• Glycated molecules  Matrix deposition in basal lamina underlying endothelium and in mesangial matrix
No immune complex
What is the clinical diagnosis

A

Diabetic Nephropathy

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14
Q

• Female, 50 years old
• Unwell for 3 weeks
• Cough
• Serum biochemistry – creatinine 500 (was 60 one year before)
• Rapidly rising creatinine = acute renal failure
• Ultrasound: no renal tract lesion
• Check clotting then renal biopsy: early endothelial damage with fibrin deposition and crescents with crushed glomerular tuft
what is the diagnosis

A

Crescentic Glomerulonephritis

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15
Q

What are the causes of Crescentic Glomerulonephritis

A
  1. Granulomatosis with polyangiitis (previously known as Wegener’s granulomatosis)
  2. Microscopic polyarteritis (a disease very much like granulomatosis with polyangiitis)
  3. Antiglomerular basement membrane disease
  4. Other - Many other forms of glomerulonephritis
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16
Q

What is 1. Granulomatosis with polyangiitis (previously known as Wegener’s granulomatosis)

A

• A form of vasculitis (= inflammation in vessels) which affects vessels in kidneys, nose and lungs

17
Q

What further tests can be done to confirm Granulomatosis with polyangiitis (previously known as Wegener’s granulomatosis)

A

Serum test shows presence of anti-neutrophil cytoplasmic antibodies (ANCA)

18
Q

What is the nature of anti-neutrophil cytoplasmic antibodies (ANCA) in1. Granulomatosis with polyangiitis

A

– Not deposited in kidney
– Antibodies directed against proteinase 3 and myeloperoxidase, 2 enzymes in primary granules of neutrophils
– Antibodies produce tissue damage via interactions with primed neutrophils and endothelial cells.
– Form of autoimmunit

19
Q

What is the prognosis for 1. Granulomatosis with polyangiitis

A

– Fatal (mean survival 6 months) if left untreated

– Cyclophosphamide – 75% complete remission- anti-cancer drug