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ZA - Renal System > Clinical Aspects of Glomerular Disease (Glomerulonephritis) > Flashcards

Clinical Aspects of Glomerular Disease (Glomerulonephritis) Flashcards

1
Q

What is glomerulonephritis?

A

A group of inflammatory disorders of the kidney

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2
Q

How are the different sub-types of GN classfied?

A

Via their morphology

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3
Q

Describe nephrotic syndrome.

A

Massive loss of protein via urine = Hypoalbuminaemia - this is due to leaky glomeruli

Hypoalbuminaemia leads to oedema and hyperlipidaemia

Urine looks frothy

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4
Q

Why does Hypoalbuminaemia cause oedema and hyperlipidaemia?

A

Oedema - loss of albumin causes a reduced intravascular oncotic pressure which causes fluid to leak out of vessels and into surrounding tissue

Hyperlipidaemia - low albumin causes liver to increase albumin production in order to compensate BUT this also leads to increased production of lipids

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5
Q

Describe nephritic syndrome.

A

High levels of blood in urine
Increased levels of protein, but not as high as in nephrotic
Mild hypertension
Low urine volume due to reduced renal function

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6
Q

What type of glomerulonephritis causes nephrotic syndrome?

A

Non-proliferative glomerulonephritis - such as minimal change, membranous, focal segmental and Membranoproliferative (not sure about this one)

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7
Q

What type of glomerulonephritis causes nephritic syndrome?

A

Proliferative glomerulonephritis - such as:

IgA
Cresent/rapidly progressive
Post-streptococcal/post-infective

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8
Q

What do diffuse, focal, global and segmental mean in terms of glomerulonephritis?

A

Focal affects under 50% of the glomeruli
Diffuse affects over 50%
Global affects 100%

Segmental only affects specific parts of the glomerulus

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9
Q

Differentials for nephrotic syndrome?

A

Congestive heart failure

Hepatic disease

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10
Q

Name the proliferative subtypes again and name which ones are focal and which on is diffuse.

A

IgA - focal

Post Infectiive - diffuse

Crescentic/Focal necrotizing/rapidly progressive - focal

Membrano-proliferative

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11
Q

Describe the presentation of post-infective GN.

A

Follows 10-21 days after infection of throat or skin

Patient will be generally unwell and have dark urine

Might have puffy face
Might have higher BP

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12
Q

Most common type of bacteria causing post-infective GN?

A

Lancefield group A streptococci

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13
Q

Does post-infective GN have a genetic predisposition?

A

Yes

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14
Q

Treatment for post-infective GN?

A

Loop diuretics IF there is oedema - frusemide

Vasodilators for mild hypertension - amlodipine

Antibiotics are debatable

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15
Q

Most commonest cause of GN ?

A

IgA nephropathy

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16
Q

Pathogenesis of IgA GN?

A

IgA is depositied in mesangium causing mesangial proliferation (see Dr P Browns lecture for more)

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17
Q

How will IgA present?

A

As a nephritic syndrome but with microscopic blood in urine with maybe some protein present in urine also

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18
Q

IgA investigations?

A

Biopsy will show IgA deposits

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19
Q

IgA GN treatment?

A

Steroids or cyclophosphamide if reduced renal function - support for transplantation

Otherwise just support symptoms, like hypertension with hypertensive therapy (ACEIs)

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20
Q

What is the outcome for IgA?

A

20% ~ reach ESRD in 20 years

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21
Q

Outcomes for post infective?

A

95% of children make full recovery

The rest could go on to develop crescentic/ rapid progressing GN

22
Q

Describe Cresentic GN.

A

Most aggressive type and can lead to ESRD in days

23
Q

What does crescentic look like pathology wise?

A

A crescent shape of cells fills the bowmans space

24
Q

What does crescentic GN do to creatinine levels?

A

Increases them greatly

25
Q

What is anti-GBM?

A

Anti-glomerular basement membrane also known as goodpastures

A type of crescentic GN causes by anti-GBM (glomerular basement membrane)

26
Q

What % of crescentic GN is anti-GBM?

A

10-20%

27
Q

How does anti-GBM present?

A

Nephritis

Haematuria and haemoptysis

28
Q

What causes the haemoptysis in anti-GBM?

A

A CxR will show infiltrates

29
Q

How is anti-GBM diagnosed?

A

Anti-GBM antibodies in serum and kidney will be detected

30
Q

Treatment for anti-GBM?

A

Agressive immunosuppression - steroids, plasma exchange, cyclophophamide

31
Q

How is crescentic GN managed?

A

Same as anti-GBM

Immunosupression

32
Q

Name some ways to immunosupress.

A 
Steroids
Cyclophosphamide
Plasma exchange
B-cell therapy 
Complement inhibitors
33
Q

Crescentic prognosis?

A

Good if treated early

34
Q

Summarise proliferative GN.

A

Presents with nephritic syndrome
Blood on dipstix with variable proteinuria
Can cause rapid decline in renal function –> dialysis
Early diagnosis and treatment = good prognosis

35
Q

What actually is the main difference between proliferative and non-p?

A

P - Excessive numbers of cells in glomeruli. These include infiltrating leucocytes

Non-P = Glomeruli look normal or have some areas of scarring. Normal no. of cells

36
Q

Name again the types on non-p GN?

A

Minimal change
Membranous
Focal and sentimental
Membranoproliferative (not sure again if this is P or NP)

37
Q

How do we generally manage nephrotic syndrome?

A

Treat oedema via loop diuretics/salt and fluid restriction

Treat hypertension - RAAS blockade

Treat hyperlipidaemia - statins

Reduce risk of thrombosis - Heparin/Warfarin

Reduce risk of infection - pnumonococcal vaccines

38
Q

What is the commonest cause of nephrotic syndrome in children?

A

Minimal change GN

39
Q

Describe the onset of minimal change GN.

A

Sudden onset of oedema within days

40
Q

Treatment for minimal change GN?

A

Steroids - prednisolone until remission is achieved then slowly taper off

2/3rds of patients relapse so treat this with a further steroid course

Any further relapses trat with cyclophosphamide

41
Q

Minimal change prognosis?

A

Despite replases prognosis is good and risk of ESRD is low

Steroid toxicity risk is high depending on exposure

42
Q

Describe focal and segmental GN.

A

Is not a single disease but a syndrome with multiple causes

Can be 1y - idiopathic - or have a 2y cause

Presents with nephrotic syndrome

High chance of progression to ESRD

43
Q

What does the pathology show for focal segmental GN?

A

Reveals focal and segmental sclerosis with distinctive patterns

44
Q

Is steroids a good treatment for FS GN?

A

No as it is generally resistant to steroids

45
Q

Treatment for FSGN?

A

General measures to handle symptoms - hypertension, hyperlipidaemia, oedmea, and anti-coagulants

Trail steroid treatment - even if it partially works it still improves prognosis

Could try cyclophosphamide, cyclosporin etc

46
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous nephropathy

47
Q

What causes the majority of membranous GN cases?

A

Occur in isolation - idiopathic

48
Q

What are the serological markers for membranous GN?

A

Anti-phospholipase A2 receptor antibody

Thrombospondin type 1 domain containing 7A

49
Q

2y causes of membranous GN?

A

Malignancy
SLE
Rheumatoid arthritis
Drugs - NSAIDs, gold, penicillamine

50
Q

Treatment for membranous GN?

A

General measures for ~6 months

Immunosuppression if symptomatic nephrotic syndrome - rising proteinuria/deteriorating renal function

Cyclophosphamide and steroids, alternate months for 6 months

Cyclosporin

Rituximab - b-cell therapy

51
Q

Prognosis of membranous GN?

A

Resolves in 1/3 of patients
Prognosis good if treatment controls the proteinuria

BUT

~25% end up on dialysis in 10 years and it can reoccur even after transplantation

52
Q

Summarize the key points for non-proliferative GN.

A

Presents as nephrotic syndrome
Renal biopsy is a key investigation
ID the cause and treat it if 2y
General measures to control symptoms are important in all cases
Specific treatment should be tailored to the type of GN

ZA - Renal System (27 decks)

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