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Systems: Urinary AB > Glomerular Disease > Flashcards

Glomerular Disease Flashcards

1
Q

How does a normal glomerulus function?

A
  • Blood enters via afferent arteriole
  • Blood is filtered across glomerular membrane
  • All proteins equal to or larger than albumin (including immunoglobulins) will not be filtered- they will stay in the plasma)
  • Filtrate goes into Bowman’s space then into proximal tubule
  • Blood cells, some fluid and albumin and larger proteins exit via efferent arteriole
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2
Q

What cells wrap around the capillaries present in the glomerulus?

A

Podocytes

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3
Q

How are podocytes able to wrap around capillaries?

A

They have interdigitating fingers or foot processes

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4
Q

What are the 3 components of the filter barrier (membrane)?

A
  • Endothelial cell cytoplasm
  • Basal lamina
  • Podocyte
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5
Q

What are mesangial cells?

A

Tree-like group of cells which support capillaries

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6
Q

What is present in the efferent arteriole of the glomerulus?

A

Contains plasma including unfiltered proteins such as albumin and antibodies

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7
Q

What is glomerulonephritis?

A
  • Diseases of the glomerulus which can be inflammatory or non inflammatory
  • Large range of conditions
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8
Q

What does primary glomerulonephritis affect?

A

Only affects the glomerulus

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9
Q

What does secondary glomerulonephritis affect?

A

Glomerulus and other parts of the body e.g. in SLE or Wegener’s

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10
Q

What is the aetiology of glomerulonephritis?

A
  • Some are due to immunoglobulin deposition

- Some are diseases with no immunoglobulin deposition - for example- diabetic glomerular disease

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11
Q

What are 4 common presentations of glomerulonephritis?

A
  • Haematuria (blood in the urine)
  • Heavy proteinuria (nephrotic syndrome)
  • Slowly increasing proteinuria
  • Acute renal failure (rapidly rising creatinine)
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12
Q

What are the main causes of glomerulonephritis?

A
  • UTI
  • Urinary tract stone
  • Urinary tract tumour
  • Glomerulonephritis
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13
Q

What must be done before a renal biopsy can be carried out?

A

Check clotting

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14
Q

What may the initial presentation of IgA proliferative nephropathy?

A

Discoloured urine (due to presence of blood)

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15
Q

What investigations may be carried out for IgA proliferative nephropathy?

A
  • Dipstick urine
  • Urine culture
  • Ultrasound of abdomen
  • Renal biopsy
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16
Q

What may be found on histology of IgA proliferative nephropathy?

A
  • Accumulation of pink mesangial matrix
  • Too many mesangial cells
  • Deposits of IgA with prominent of mesangial cells
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17
Q

What may be seen on immunofluorescence of IgA proliferative nephropathy?

A

Immunoglobulin (of IgA type) and complement component C3 in mesangial area of all glomeruli

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18
Q

Why is there increased mesangial cells in IgA proliferative nephropathy?

A

IgA deposits cause increased proliferation of mesangial cells

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19
Q

What is the aetiology of IgA glomerulonephritis?

A

-Unknown
-May be due to excess antibody production as excess antibody (IgA) sometimes present in serum, but this is also true of some people who do not have IgA glomerulonephritis
n

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20
Q

Why is IgA not removed by the glomerulus?

A

It is not known why but it is probable very important to the cause of the disease

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21
Q

Does IgA get filtered into the urine?

A

No, the IgA is stuck within the mesangium

22
Q

What part of the glomerulus becomes clogged with IgA?

A

The filter NOT the mesangium

23
Q

Why does IgA blocking the filter of the glomerulus lead to red cells escaping into the urine?

A

This is not known

24
Q

Why do mesangial cells produce more matrix in IgA proliferative nephropathy?

A

IgA irritates mesangial cells and causes them to proliferate and produce more matrix

25
Q

What is the prognosis of IgA nephropathy?

A
  • Usually self limiting

- Small % go onto develop chronic renal failure (via continued deposition of matrix)

26
Q

How may nephrotic syndrome present?

A

Oedema, particularly of the legs

27
Q

What investigations should be carried out for nephrotic syndrome?

A
  • Blood biochemistry and haematology tests
  • Urine dipstick
  • Renal biopsy
28
Q

What may be found on blood tests of nephrotic syndrome??

A

Serum albumin low

29
Q

What may be found on urine dipstick of nephrotic syndrome?

A

Proteinuria

30
Q

What may found in the urine in nephrotic syndrome?

A

Protein (albumin) -very heavy loss

31
Q

What must be true for a clinical diagnosis of nephrotic syndrome?

A

Must be abnormality of glomerular filter

32
Q

What may be seen on histology of membranous glomerulonephritis?

A
  • Thickened glomerular basement membrane
  • Spikes of new basement membrane matrix material underneath podocytes
  • Deposits of IgG
33
Q

What happens to antibody and albumin with a normal basement membrane?

A

They stay in the plasma. They are NOT filtered

34
Q

How does IgG become stuck in the membrane?

A

IgG deposits itself between basal lamina and podocyte but cannot go further and is not filtered into urine

35
Q

How does albumin get filtered into the urine in membranous glomerulonephritis?

A
  • IgG is too big to be filtered into urine, but IgG activates complement (C3), which punches holes in filter
  • Leaky filter now allows albumin to be filtered into urine causing nephrotic syndrome
36
Q

What is the prognosis of membranous glomerulonephritis?

A

-1/4 in chronic renal failure within 10 years

37
Q

What is the underlying cause of IgG production and accumulation in membranous glomerulonephritis?

A
  • Unknown but can sometimes have underlying malignancy

- In many patients antigen is phospholipase A2 receptor but it is unknown why

38
Q

What is the pathology behind diabetic nephropathy?

A
  • Glycated molecules
  • Matrix deposition in basal lamina underlying endothelium and In mesangial matrix
  • Thickened but leaky basement membranes and mesangial matrix compresses capillaries (no immune complexes)
39
Q

What may be seen on histology of diabetic nephropathy?

A
  • Small compressed capillary lumen
  • Thickened capillary wall
  • Increased mesangial matrix
  • Thickened narrowed arterioles
  • Adhesions to Bowman’s capsule
40
Q

What are Kimmelsteil Wilson lesions?

A

Gross excess of mesangial matrix forming nodules that is characteristic of diabetic nephropathy

41
Q

What is the prognosis of diabetic nephropathy?

A
  • Inevitable decline if established diabetic nephropathy and if continued poor diabetic control
  • Damage can be arrested but not reversed
42
Q

What will be evident on serum biochemistry of AKI?

A

Rapidly rising creatinine

43
Q

What may be seen on histology of crescentic glomerulonephritis?

A
  • Early endothelial damage with fibrin deposition

- Cellular proliferation and influx of macrophage (=crescent) around glomerular tuft, within Bowman’s space

44
Q

What can cause a crescentic glomerulonephritis pattern of injury?

A
  • Granulomatosis with polyangiitis (also known as Wegener’s granulomatosis)
  • Microscopic polyarteritis (a disease very much like Wegeners)
  • Antiglomerular basement membrane disease
  • Many other forms of glomerulonephritis
45
Q

What is granulomatosis with polyangiitis?

A

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

46
Q

What test should be done with Wegener’s granulomatosis?

A

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

47
Q

Where are ANCA not deposited?

A

Not deposited in the kidneys

48
Q

What is ANCA directed against?

A

Antibodies directed against proteinase 3 and myeloperoxidase, 2 enzymes in primary granules of neutrophils

49
Q

What does ANCA produce?

A

Antibodies produce tissue damage via interactions with primed neutrophils and endothelial cells.

50
Q

Why do ANCA form?

A

Unknown at present. Perhaps a form of autoimmunity

51
Q

What is the prognosis of Wegener’s?

A
  • Fatal (mean survival 6 months) if left untreated

- Cyclophosphamide (treatment) – 75% complete remission

Systems: Urinary AB (26 decks)

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