Lecture 15 - Glomerular pathology Flashcards

1
Q

Focal

A

Less than 50% of the glomeruli affected

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2
Q

Segmental

A

Part of the glomerular tuft affected

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3
Q

Membranous

A

Thickening of the glomerular capillary wall

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4
Q

Crescent

A

Accumulation of cells within the Bowman’s capsule

Compress glomerulus

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5
Q

Specialised structures of the glomerulus

A
Mesangial cells
Juxtaglomerular apparatus
Podocytes
-vely charged basement membrane 
Fenestrated endothelium
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6
Q

Nephrotic syndrome cardinal signs

A

Proteinurea - frothy urine
Hypoablumineamia
Oedema

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7
Q

Hypercholesteraemia and hyperlipidaemia

A

Seen in nephrotic syndrome due to decreased production of apolipoproteins due to proetinuria

Liver makes albumin to compensate and also produces lipids

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8
Q

Nephrotic syndrome location

A

Podocytes
Subepithelial damage
GBM - decreased filtration allowing proteins to be filtered

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9
Q

Primary causes of nephrotic syndrome

A

Minimal change glomerulonephritis
Focal segmental glomerulosclerosis
Membranous glomerulonephritis

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10
Q

Secondary causes of nephrotic syndrome

A

Diabetic nephropathy

Systemic lupus erythromatous

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11
Q

Minimal change glomerulonephritis

A

Seen in children

Does not progress to renal failure

Unknown circulating factor that causes acute podocyte damage - nephrotic syndrome

  • intact GBM (use silver stain)

Treatment: steroids
Relapse if treatment is stopped

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12
Q

Focal segmental glomerulosclerosis

A
  • Seen in adults
  • Can progress to renal failure
  • Unknown circulating factor damaging podocytes causing scarring and decreased GFR due to glomerulosclerosis
  • Less responsive to steroids
  • Cannot give renal transplant because circulating factor still circulating
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13
Q

Membranous glomerulonephritis

A

Most common
Affects individuals of any age

  1. IgG antibody is produced against podocytes
  2. The antibody forms immune complexes with the podocyte antigen
  3. Immune complexes deposited in glomerulus as not filtered
  4. Activates compliment cascade causing inflammation
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14
Q

Prognosis of Membranous glomerulonephritis

A

1/3rd get better
1/3rd no change
1/3rd progress to renal failure

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15
Q

Membranous glomerulonephritis histology

A

Immune deposits

GBM spikes

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16
Q

Diabetic nephropathy

A
1 - Hyperglycaemia
2 - Glycation of proteins in the GBM 
3 - Thickened GBM wall 
4 - hyaline arteriosclerosis
5 - glomerular hypertension 
6 - Increased GFR
7 - Hyperfiltration
17
Q

Kimmel wilson nodules

A
  1. Glycation of proteins
  2. Increases cytokines
  3. Mesangial expansion
  4. Kimmel Wilson nodules - deposits of proteins
  5. Vessels expand further with bigger filtration slits so more leaky
18
Q

Diabetic nephropathy stages

A

Hyperfiltration
Microalbuminuria
Overt proteinuria - decreased GFR irreversible
ESRD

19
Q

How does diabetic nephropathy cause glomerular hypertension ?

A
  1. Glycation of proteins
  2. SGLT2 upregulated
  3. Reduced Na+ to macula densa stimulating the afferent arteriole to dilate and RAAS
  4. Efferent arteriole constricts
20
Q

Nephritic syndrome cardinal features

A

Haematuria
Hypertension
Oliguria

21
Q

Causes of nephritic syndrome

A

Goodpasture’s syndrome
ANCA vasculitis
SLE

Hameaturia:
IgA nephropathy
Alport’s syndrome

22
Q

Pathphysiology of nephritic syndrome

A
  1. Inflammation of glomerulus
  2. Infiltration of GBM by immune cells may form platelet plug in endothelial cells
  3. Renal plasma flow drops
  4. Reduced GFR
23
Q

What does reduced GFR cause in nephritic syndrome?

A

Oliguria - less urine filtered
Azotemia - nitrous containing waste products are not properly filtered
Hypertension - RAAS activated

24
Q

How is nephritic syndrome managed?

A

Treat underlying cause
Treat oedema - diuretics
BP control - ACE inhibitors, angiotensin receptor blockers and salt restriction

25
Q

Goodpasture’s syndrome

A

Anti - GBM disease

  • Body produces antibodies against the GBM where collagen IV affected.
  • Large holes are created which causes hyperfiltration
  • Rapidly progresses to acute severe nephritic syndrome - Type 3 sensitivity reaction

Treatment:

  • Immunosuppression
  • Plasmapheresis (filter blood of the antibody)
26
Q

ANCA vasculitis

A

Caused by anti-neutrophilic cytoplasmic autoantibody (ANCA)

  • binds to and activates neutrophils
  • Activated neutrophils attack small blood vessels which can include the glomerulus
  • Develops into nephritic syndrome

Treatments:

  • Immunosuppression
  • Plasmapheresis (filter blood of the antibody)

Histologically: crescent segmental necrosis of glomerulus

27
Q

IgA nephropathy

A

Occurs at any age
Occurs in mesangial cells
MOST COMMON cause of glomerulonephritis and most progresses to renal failure

Immune complexes formed with galactose deficient IgA deposits in the glomerulus mesangial cells as it cannot be filtered.

Stimulates compliment pathway and inflammation

28
Q

Alports syndrome

A

X linked autosomal recessive
Hereditary defective collagen IV
Associated with deafness

GBM already has holes

29
Q

What is damaged in glomerulonephritis?

A
  1. Capillary endothelium
  2. GBM
  3. Mesangial cells
  4. Podocytes