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US > Session 8: Glomerular Pathology > Flashcards

Session 8: Glomerular Pathology Flashcards

1
Q

Give examples of where glomerular damage might occur in within the glomerulus.

A

Subendothelial damage

Glomerular basement membrane damage

Subepithelial damage and damage to podocytes

Mesangial damage and paramesangial damage

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2
Q

Why is it important to know where the damage in the glomerulus has occured?

A

Because the site of glomerular injury will determine the clinical presenation of the condition.

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3
Q

How can you determine where the damage has occurred in the glomerulus?

A

By biopsy and then light microscopy to investigate the histology.

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4
Q

Give examples of histological apperances in glomerular conditions.

A

Focal

Diffuse

Segmental

Global

Membranous

Proliferative

Crescent

Glomerulosclerosis

Glomerulonephritis

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5
Q

Explain focal pathology

A

Involving less than 50% of the glomerulus on light microscopy

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6
Q

Explain diffuse pathology

A

Involving more than 50% of glomerulus on LM

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7
Q

Explain segmental pathology

A

Involving part of the glomerular tuft

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8
Q

Explain global pathology

A

Involving the entire glomerular tuft

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9
Q

Explain membranous pathology

A

Thickening of the glomerular capillary wall

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10
Q

Explain proliferative pathology

A

Increased number of cells in the glomerulus. These can either be glomerular cells or invading inflammatory cells.

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11
Q

Explain crescent pathology

A

Accumulation of cells in the Bowman’s space

(Associated with more severe disease)

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12
Q

Explain glomerulosclerosis pathology appearance

A

Segmental or global capillary collapse. No filtration occuring at the sclerotic area

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13
Q

Explain glomerulonephritis pathology appearance

A

Any condition associated with inflammation of the glomerular tuft

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14
Q

What is nephrotic syndrome?

A

A triad of symptoms involving damage of the subepithelial region and specifically to the podocytes of the glomerulus. The podocytes are responsible for fine filtration and selectivity of substances across the glomerulus and into the tubular duct.

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15
Q

What is the triad of symptoms in nephrotic syndrome?

A

Proteinuria of over 350mg/mmol in 24 hours

Hypoalbuminaemia

Oedema

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16
Q

Explain the pathophysiology of nephrotic syndrome.

A

Podocyte damage leads to less selectivity of the glomerular filtration barrier. This leads to an increase in number of proteins being able to enter the tubular lumen. A large amount of these proteins will be albumin.

This leads to a decreased concentration of albumin in the blood leading to lower capillary oncotic pressure. As the oncotic pressure has decreased the net force between the capillary oncotic pressure, the capillary hydrostatic pressure and the hydrostatic interstitial pressure has now changed.

This leads to the oedema. Commonly the oedema can be found peripheral in hands and feet as well as periorbital oedema.

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17
Q

State of GFR and blood pressure in nephrotic syndrome.

A

Usually normal

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18
Q

Give another common clinical presenation of nephrotic disease that isn’t included in the triad of symptoms.

A

Hyperlipidaemia

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19
Q

Explain why hyperlipidaemia might occur in nephrotic syndrome.

A

As the albumin is low the liver will start to produce more albumin to compensate.

It is thought that this mechanism is accompanied by hepatic synthesis of lipids (cholesterol) as well.

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20
Q

Give common primary causes of nephrotic syndrome.

A

Minimal Change Glomerulonephritis

Focal Segmental Glomerulosclerosis (FSGS)

Membranous Glomerulonephritis

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21
Q

Give common secondary causes of nephrotic syndrome.

A

Diabetes Mellitus (T1 &T2)

Renal amyloidosis

Connective tissue disorders such as Systematic Erythematous Lupus (SLE)

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22
Q

Age group of Minimal Change Glomerulonephritis.

A

Childhood/Adolescence with a reduced incidence in increasing ages

23
Q

Treatment of MCG

A

Usually responds to steroids

24
Q

Progression to renal failure in MCG?

A

Not common

25
Q

Histological appearance of MCG.

A

Minimal and sometimes negligible changes hence its name Minimal Change Glomerulonephritis

However on electron transmission microscopy you might find that there is absence of podocytes

26
Q

Pathogenesis of MCG.

A

Unknown but thought to be a circulating factor damaging the podocytes.

This is because it seems to be something wrong with the blood as blood transfusions has caused MCG

27
Q

Age group of Focal Segmental Glomerulosclerosis (FSGS)

A

Adults

28
Q

Difference between MCG and FSGS

A

FSGS is not normally found in children and adolescence, more commonly found in adults.

FSGS is less responsive to steroids.

FSGS expresses glomerulosclerosis.

FSGS more commonly progresses to renal failure.

29
Q

Pathogenesis of FSGS.

A

Unknown as well. Thought to be a circulating factor damaging podocytes.

30
Q

Which is the most common primary cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis

31
Q

What is special in Membranous glomerulonephritis compared to MCG and FSGS?

A

That is is due to immune complex deposits and thus probably autoimmune.

32
Q

What might membranous glomerulonephritis be secondary to?

A

Other pathologies like lymphoma

33
Q

What is nephritic syndrome?

A

Not to be confused with nephrotic syndrome. It is an inflammation of the glomerulus expressing a triad of symptoms.

34
Q

What is the triad of symptoms in nephritic syndrome?

A

Haematuria

Hypertension

Reduced GFR

35
Q

Explain the pathophysiology in nephritic syndrome.

A

There is inflammation of the glomerular capillaries. This leads to leaky capillaries as the consequence of the inflammatory process.

This means that erythrocytes (haematuria) and leukocytes (pyuria) can escape and enter the tubular lumen.

There are however still podocytes so the selectivity has not decreased so the proteinuria is rather mild.

The inflammation also damage the glomerulus as a whole and will lead to reduced GFR as well as oliguria with azotemia.

36
Q

Give causes of nephritic syndrome.

A

IgA nephropathy also called Berger’s disease

Anti-GBM disease also called Goodpasture syndrome

ANCA - Vasculitis

Alport Syndrome

Thin glomerular basement membrane disease

SLE

Acute proliferative glomerulonephritis

Rapidly progressive glomerulonephritis

37
Q

Most common cause of nephrotic syndrome.

A

IgA Nephropathy

38
Q

Age group of IgA nephropathy.

A

Any age.

39
Q

Classical presentation of IgA nephropathy.

A

Visible or invisible haematuria.

Mucosal infections (hence IgA)

+/- proteinuria

Significant proportion progressing to renal failure.

40
Q

Treatment of IgA nephropathy.

A

No effective treatment

41
Q

Histological appearance of IgA nephropathy.

A

Usually mesangial damageas the IgA can reach the mesangium and deposit to damage it.

42
Q

Pathogenesis of IgA nephropathy.

A

Deposition of circulating IgA containing immune complexes in the glomerulus.

43
Q

Give examples of hereditary nephropathies.

A

Thin GBM nephropathy

Beningn familial nephropathy

Isolated haematuria

Thin GBM

Alport Syndrome

44
Q

What is Alport syndrome?

A

X-linked recessive disease where there is abnormal collagen IV found. This causes abnormal appearance of the GBM where it is split and laminated.

45
Q

Classical presentation of Alport Syndrome.

A

Ear problems (deafness)

Eye problems

Kidneys problems progressing to renal failure

46
Q

Explain what Anti-GBM aka Goodpasture syndrome is.

A

A relatively uncommon but important syndrome. This is because it is a rapidly progressive glomerulonephritis that can cause acute onset of severe nephritic syndrome and end stage renal failure.

47
Q

What clinical presentation is anti-GBM commonly associated with?

A

Pulmonary haemorrhage.

48
Q

What causes anti-GBM?

A

Autoantibody to collagen IV in the basement membrane of the glomerulus.

49
Q

Treatment of anti-GBM.

A

Treatable by immunosuppression and plasmaphoresis.

This is however only possible if the condition has been caught early.

50
Q

What is vasculitis?

A

A group of systemic disorders where there is no immune complex or antibody deposition.

It is however associated with Anti Neutrophil Cytoplasmic Antibody and also called ANCA-Vasculitis.

It can cause nephritic syndrome.

51
Q

Treatment of ANCA-vasculitis.

A

Glucocorticoids like prednisolone.

It is treatable if caught early.

52
Q

Histological presentation of ANCA-vasculitis.

A

Segmental necrosis and crescent.

53
Q
A

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