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Y2 Renal > Glomerular disease > Flashcards

Glomerular disease Flashcards

1
Q

What is glomerulonephritis

A

Inflammation of or around the glomerulus and nephron

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2
Q

What can all forms of glomerulonephritis lead to

A

Nephritic / nephrotic syndrome
Different forms have tendency to cause one or the other or mixed

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3
Q

What are the features of nephritic syndrome

A

Haematuria
Red cell casts in urine (microscopic bleeding)
Hypertension
Mild to moderate proteinuria
Oliguria

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4
Q

What are the features of nephrotic syndrome

A

Massive proteinuria >3.5g/day
Hypoalbuminaemia
Oedema
Hypercoagulability
Hyperlipidaemia
Low total thyroxine levels

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5
Q

How does nephrotic syndrome predispose patients to thrombosis

A

Due to loss of antithrombin-III proteins and rise in fibrinogen levels

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6
Q

Why may low total thyroxine levels be seen in nephrotic syndrome

A

Due to loss of thyroxine binding globulin proteins

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7
Q

What are the symptoms of nephritic syndrome

A

Haematuria
Oedema (to a lesser extent compared to nephrotic syndrome)
Oliguria
Uraemic symptoms - fatigue, reduced appetite, pruritus

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8
Q

What are the symptoms of nephrotic syndrome

A

Facial oedema
Peripheral oedema
Frothy urine (due to heavy proteinuria)
Fatigue
Recurrent infections
Hypercoagulability -> MI / DVT / renal vein thrombosis

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9
Q

Why are patients with nephrotic syndrome predisposed to recurrent infections

A

Due to loss of immunoglobulins

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10
Q

Why is oedema more severe in nephrotic syndrome

A

Due to heavy loss of protein in urine causing hypoalbuminaemia.
Hypoalbuminaemia causes oedema because of reduced oncotic pressure so water goes out of blood vessels and into tissues

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11
Q

Clinical signs of nephrotic syndrome

A

Periorbital oedema / lower limbs oedema / Ascites
SOB due to pleural effusion
Xanthelasma due to hyperlipidaemia

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12
Q

Differences between nephritic and nephrotic syndrome

A

Nephritic syndrome causes haematuria, oliguria, hypertension whereas nephrotic syndrome does not

Nephrotic syndrome causes HEAVY proteinuria > 3.5 whereas proteinuria in nephritic syndrome is mild to moderate

Nephrotic syndrome causes more severe oedema

Nephrotic syndrome causes hyperlipidaemia and hyper coagulability whereas nephritic syndrome does not

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13
Q

What are the different types of glomerulonephritis

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous GN
IgA nephropathy
Post-infectious GN
Membranoproliferative
Rapidly progressive GN
Goodpasture’s syndrome
Alport’s syndrome

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14
Q

Which form of GN is the most common

A

IgA nephropathy

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15
Q

What are the types of GN regarding to its pathophysiology

A

Proliferative
Non-proliferative

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16
Q

What is proliferative GN

A

Presence of proliferation of endothelial and mesangial cells

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17
Q

Proliferative GN typically presents with

A

Nephritic syndrome

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18
Q

What is non-proliferative GN

A

Non-proliferative process.
Due to damage to podocytes

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19
Q

Non-proliferative GN typically presents with

A

Nephrotic syndrome

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20
Q

Which types of GN are non-proliferative

A

Minimal change
Focal segmental
Membranous GN

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21
Q

Which types of GN are proliferative

A

IgA nephropathy
Rapidly progressive GN
Anti-glomerular basement membrane antibody disease
Vasculitic disorders - GPA, MPA

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22
Q

Which types of GN can cause mixed- nephritic and nephrotic syndrome

A

Membranoproliferative GN
Post-Strep (infectious) GN

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23
Q

Minimal change disease is the most common

A

Most common cause of nephrotic syndrome in children

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24
Q

Causes of minimal change disease

A

Mostly idiopathic

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25
Q

What are the typical investigation results for minimal change disease

A

Highly selective proteinuria
NORMAL renal biopsy under light microscopy
NORMAL BP
Electron microscopy shows fusion of foot processes

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26
Q

What does highly selective proteinuria mean in minimal change disease

A

Only intermediate sized proteins such as albumin can leak through

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27
Q

What is special about minimal change disease

A

Normal light microscopy results
Abnormality only seen on electron microscopy

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28
Q

Management of minimal change disease

A

Oral corticosteroids (80% are responsive)
Cyclophosphamide for steroid-resistant cases
Salt restriction and fluid management

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29
Q

Describe the prognosis of minimal change disease

A

Relapse is common
1/3 have only 1 episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood

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30
Q

Focal segmental glomerulosclerosis is the most common

A

Cause of nephrotic syndrome in adults - young adults

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31
Q

Causes of focal segmental glomerulosclerosis

A

Idiopathic
Secondary causes
- HIV
- SLE
- reflux nephropathy
- sickle cell disease
- heroin

32
Q

Typical investigation results for focal segmental glomerulosclerosis

A

On light microscopy - mesangial collapse and sclerosis
On electron microscopy - fusion of foot processes

33
Q

Management of focal segmental glomerulosclerosis

A

Salt restriction and fluid management
Prolonged Steroids
Cyclophosphamide

34
Q

Describe the prognosis of focal segmental glomerulosclerosis

A

60% go into remission with prolonged steroids
40% process into end stage renal failure after 10 years

35
Q

Membranous glomerulonephritis mostly causes

A

nephrotic syndrome in adults (2nd most common cause)

36
Q

Causes of membranous glomerulonephritis

A

Mostly idiopathic
Infections - Hep B, malaria
Malignancy - Prostate, lung, lymphoma, leukaemia
Drugs
SLE
Thyroiditis

37
Q

What infections are associated with membranous glomerulonephritis

A

Hep B
Malaria

38
Q

What malignancies are associated with membranous glomerulonephritis

A

Prostate
Lungs
Lymphoma
Leukaemia

39
Q

What drugs are associated with membranous glomerulonephritis

A

Gold
Penicillamine
NSAID

40
Q

Typical investigation results for membranous glomerulonephritis

A

Light microscopy
- thickened glomerular basement membrane
Immunofluorescence
- diffuse uptake of IgG
EM
- thickened glomerular basement membrane with sub epithelial deposits of immune complexes

41
Q

What is the classic sign of membranous glomerulonephritis in EM

A

Spike and dome appearance due to subepithelial deposits

42
Q

Management of membranous glomerulonephritis

A

all patients should receive ACEi / ARB
Steroids + cyclophosphamide

43
Q

Describe the prognosis of membranous glomerulonephritis

A

Rule of thirds
- 1/3 spontaneous remission
- 1/3 chronic MGN
- 1/3 develop end stage renal failure

44
Q

Membranoproliferative GN causes nephritic / nephrotic/ mixed syndrome

A

Mixed

45
Q

Causes of membranoproliferative GN

A

Mostly idiopathic
Hep C
SLE

46
Q

Typical investigation results of membranoproliferative GN

A

Thickened basement membrane
Thickened mesangium
Subendothelial deposition of IgG

47
Q

What is the classic appearance of membranoproliferative GN

A

Tram tracking appearance due to deposits and thickened mesangium (mesangial cells disperse themselves between the basement membrane and endothelium as well)

48
Q

Management of membranoproliferative GN

A

Steroids for children
Dipyridamole and aspirin for adults
Kidney transplantation for ESRF

49
Q

Cause of IgA nephropathy

A

Due to mesangial deposition of IgA immune complexes

50
Q

IgA nephropathy is associated with

A

URTI
Henoch Schonlein purpura
Dermatitis herpetiformis
Coeliac
Cirrhosis

51
Q

What is the classic presentation of IgA nephropathy

A

Macroscopic haematuria in young people after a URTI

52
Q

IgA nephropathy causes nephritic / nephrotic / mixed syndrome

A

Nephritic syndrome

53
Q

Typical investigation results for IgA nephropathy

A

LM
- mesangial cell proliferation
Immunofluorescence
- IgA deposits in mesangium
EM
- deposits in mesangium

54
Q

How long does GN occur after URTI in IgA nephropathy

A

1-2 days

55
Q

Management of IgA nephropathy

A

If only haematuria and no/mild proteinuria
= no treatment, regular checkups
If persistent proteinuria
= ACEi/ARB
If GFR is falling / failure to respond to ACEi
= corticosteroids

56
Q

Prognosis of IgA nephropathy

A

25% develop into ESRF

57
Q

What are the markers of poor prognosis of IgA nephropathy

A

Male
Proteinuria
Hypertension
Smoking
Hyperlipidaemia

58
Q

Which pathogen causes post-streptococcal glomerulonephritis

A

Streptococcus pyogene (group A beta haemolytic)

59
Q

Post-streptococcal glomerulonephritis most commonly affects which age group

A

Young children

60
Q

Post-streptococcal GN causes which type of syndrome

A

Mixed

61
Q

Investigations for post streptococcal GN

A

Bloods
Renal biopsy

62
Q

What do blood tests show in post-streptococcal GN

A

Raised anti-streptolysin O titre - confirms recent strep infection
low C3

63
Q

What are the Renal biopsy results suggesting post-streptococcal GN

A

LM - Endothelial proliferation
EM- Lumpy immune complex deposits
Immunofluorescence - granular / starry sky appearance

64
Q

Difference between post-streptococcal GN and IgA nephropathy

A

Post strep GN occurs 7-14 days after infection whereas IgA nephropathy occurs 1-2 days after infection

Post-strep GN causes low complement level

Post strep GN main symptom is proteinuria whereas IgA nephropathy is haematuria

65
Q

Causes of rapidly progressive GN

A

GPA
MPA
Goodpasture’s
SLE

66
Q

Rapidly progressive GN causes which type of syndrome

A

nephritic syndrome

67
Q

Investigation results for rapidly progressive GN

A

Crescent formation in glomeruli (proliferating epithelial cells)

68
Q

Management of rapidly progressive GN caused by goodpasture’s

A

high dose immunosuppression- IV methylprednisolone / cyclophosphamide
Plasmapheresis

69
Q

Management of rapidly progressive GN caused by vasculitis

A

High dose prednisolone + cyclophosphamide

70
Q

What is the defect in Alport’s syndrome

A

Defect in gene that codes for type 4 collagen causing abnormal glomerular-basement membrane

71
Q

Alport’s syndrome is more severe in

A

Males

72
Q

Mode of inheritance for Alport’s syndrome

A

Mostly X linked dominant

73
Q

Symptoms of Alpert’s syndrome

A

Microscopic haematuria
Bilateral sensorineural deafness
Lenticonus - protrusion of lens
Retinitis pigmentosa

74
Q

What is lenticonus

A

Protrusion of lens into the anterior chamber

75
Q

What is retinitis pigmentosa

A

Progressive loss of photoreceptors + retinal deposits

76
Q

Investigations of Alport’s syndrome

A

Genetic testing
Renal biopsy

77
Q

What does renal biopsy show in Alport’s syndrome

A

Longitudinal splitting of lamina dense of glomerular base membrane
Basket weave appearance

Y2 Renal (12 decks)

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