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4th year passmedicine by topic > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What are the features of nephritic syndrome?

A

Haematuria - This can be microscopic (not visible) or macroscopic (visible).

Oliguria - significantly reduced urine output.

Proteinuria is protein in the urine. In nephritic syndrome, there is less than 3g / 24 hours. Any more and it starts being classified as nephrotic syndrome.

Fluid retention

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2
Q

Hyaline casts in urine are pathonogmonic of?

A

consist of Tamm-Horsfall protein (secreted by distal convoluted tubule)
seen in normal urine, after exercise, during fever or with loop diuretics

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3
Q

brown granular casts in urine are pathonogmonic of?

A

Acute tubular necrosis

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4
Q

‘bland’ urinary sediment in urine are pathonogmonic of?

A

Prerenal uraemia

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5
Q

Red cell casts in urine are pathonogmonic of?

A

nephritic syndrome

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6
Q

What is the triad of nephrotic syndrome?

A
  1. Proteinuria (> 3g/24hr) causing
  2. Hypoalbuminaemia (< 30g/L) and
  3. Oedema
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7
Q

Why do you get an increased risk of thromboembolism in nephrotic syndrome?

A

Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis.

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8
Q

Nephrotic syndrome results in a loss of total thyroxine levels

A

true

Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels.

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9
Q

List conditions associated with nephritic syndrome

A

Rapidly progressive GN
IgA nephropathy
Alport Syndrome

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10
Q

List conditions associated with nephrotic syndrome

A 
Minimal change disease
Membranous GN
Focal segmental glomerulosclerosis
Amyloidosis
Diabetic Nephropathy
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11
Q

List conditions associated with both nephritic and nephrotic syndromes

A

Diffuse proliferative GN
Membranoproliferative GN
Post-strep GN

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12
Q

List complications of nephrotic syndrome

A

increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine- deep vein thrombosis, pulmonary embolism

renal vein thrombosis, resulting in a sudden deterioration in renal function

hyperlipidaemia
increasing risk of acute coronary syndrome, stroke etc

chronic kidney disease

increased risk of infection due to urinary immunoglobulin loss

hypocalcaemia (vitamin D and binding protein lost in urine)

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13
Q

Peak incidence of nephrotic syndrome in children?

A

between 2 and 5 years of age

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14
Q

Around 80% of cases of nephrotic syndrome in children are due to

A

minimal change glomerulonephritis

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15
Q

minimal change glomerulonephritis. generally carries a good prognosis

A

true

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16
Q

What % of cases respond to high-dose oral steroids in minimal change gn

A

90%

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17
Q

Rapidly progressive glomerulonephritis is a term used to describe

A

rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli.

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18
Q

Causes of Rapidly progressive glomerulonephritis?

A

Goodpasture’s syndrome
Wegener’s granulomatosis
others: SLE, microscopic polyarteritis

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19
Q

Features of Rapidly progressive glomerulonephritis?

A

nephritic syndrome: haematuria with red cell casts, proteinuria, oliguria

hypertension

features specific to underlying cause e.g.
haemoptysis with Goodpasture’s
vasculitic rash or sinusitis with Wegener’s

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20
Q

Commonest cause of GN worldwide?

A

IgA nephropathy

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21
Q

IgA nephropathy is also known as Berger’s disease

A

yes

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22
Q

IgA nephropathy classically presents as micro or macroscopic haemturia?

A

MACRO

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23
Q

How does IGA nephropathy classically present?

A

macroscopic haematuria in young male following an upper respiratory tract infection.

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24
Q

Associated condition with IGa nephropathy?

A

alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

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25
Q

Describe pathophysiology of iga nephropathy

A

thought to be caused by mesangial deposition of IgA immune complexes
there is considerable pathological overlap with Henoch-Schonlein purpura (HSP)
histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3

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26
Q

Iga Nephropathy never presents with nephrotic range proteinuria

A

nephrotic range proteinuria is rare

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27
Q

Renal failure is common in iga nephropathy

A

renal failure is unusual and seen in a minority of patients

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28
Q

How would ou differentiate between IgA nephropathy and post-streptococcal glomerulonephritis?

A

post-streptococcal glomerulonephritis is associated with low complement levels

main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)

there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis

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29
Q

Mainstay of management for Iga nephropathy is steroids/immunosuppressants

A

false

steroids/immunosuppressants not be shown to be useful

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30
Q

Describe markers of good prognosis in Iga nephropathy

A

frank haematuria

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31
Q

Describe markers of poor prognosis in Iga nephropathy

A 
male gender
proteinuria (especially > 2 g/day)
hypertension
smoking
hyperlipidaemia
ACE genotype DD
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32
Q

% of patients develop ESRF in Iga nephropathy

A

25%

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33
Q

What do Iga nephropathy and post streptococcal glomerulonephritis have in common

A

recent urti

haematuria

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34
Q

How is Alport’s syndrome inherited?

A

X-linked dominant pattern

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35
Q

what is alports syndrome due to

A

defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM)

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36
Q

Alports is more severe in which sex

A

males

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37
Q

Alports rarely results in renal failure

A

true

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38
Q

What is a favourite exam Q according to passmed

A

A favourite question is an Alport’s patient with a failing renal transplant. This may be caused by the presence of anti-GBM antibodies leading to a Goodpasture’s syndrome like picture.

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39
Q

Alport’s syndrome usually presents in childhood.

A

YEA

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40
Q

Describe features of alports?

A 
microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
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41
Q

Renal biopsy in alports

A

characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance
on electron microscopy

42
Q

Diagnosis of Alports

A 
molecular genetic testing
renal biopsy (electron biopsy)
43
Q

buzzword for alports

A

‘basket-weave’ appearance

44
Q

Alports can never beinherited in autosomal domiannt fashion

A

false

10-15% of cases are inherited in an autosomal recessive fashion with rare autosomal dominant variants existing

45
Q

Minimal change disease nearly always presents as which syndrome

A

nephrotic

46
Q

Minimal change disease nearly always presents as nephrotic syndrome, accounting for ?% of cases in children and ?% in adults.

A

75% of cases in children and 25% in adults.

47
Q

Causes of minimal change?

A

The majority of cases are idiopathic

In around 10-20% a cause is found:
drugs: NSAIDs, rifampicin

Hodgkin’s lymphoma
thymoma
infectious mononucleosis

48
Q

Pathophysiology of minimal change?

A

T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
the resultant reduction of electrostatic charge → increased glomerular permeability to serum albumin

49
Q

Minimal change presents with hypertension

A

false

normotension - hypertension is rare

50
Q

Minimal change has a highly selective proteinuria - describe this

A

only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus

51
Q

How do diagnose minimal change?

A

Clinical test. Biopsy only indicated if steroid resistance

52
Q

What is the test for minimal change? Findings?

A

biopsy electron microscopy shows fusion of podocytes and effacement of foot processes

normal glomeruli on light microscopy

53
Q

Management of minimal change?

A

majority of cases (80%) are steroid-responsive

cyclophosphamide is the next step for steroid-resistant cases

54
Q

Describe prognosis of minimal change?

A

1/3 have just one episode
1/3 have infrequent relapses
1/3 have frequent relapses which stop before adulthood

55
Q

Commonest glomerulonephritis in adults?

A

Membranous glomerulonephritis

56
Q

Membranous glomerulonephritis is the third most common cause of end-stage renal failure (ESRF).

A

true

57
Q

How does Membranous glomerulonephritis usually present?

A

It usually presents with nephrotic syndrome or proteinuria.

58
Q

Membranous glomerulonephritis - renal biopsy?

A

electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits.
This creates a ‘spike and dome’ appearance

59
Q

Causes of Membranous glomerulonephritis?

A

idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis

malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia

drugs: gold, penicillamine, NSAIDs

autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid

60
Q

Management of membranous GN?

A

all patients should receive an ACE inhibitor or an angiotensin II receptor blocker (ARB)

immunosupression
as many patients spontaneously improve only patient with severe or progressive disease require immunosuppression
corticosteroids alone have not been shown to be effective. A combination of corticosteroid + another agent such as cyclophosphamide is often used

consider anticoagulation for high-risk patients

61
Q

Why are ACEi / ARB used in membranous GN?

A

these have been shown to reduce proteinuria and improve prognosis

62
Q

Prognosis of membranous GN?

A

one-third: spontaneous remission
one-third: remain proteinuric
one-third: develop ESRF

63
Q

Good prognostic features for membranous GN?

A

female sex, young age at presentation and asymptomatic

proteinuria of a modest degree at the time of presentation.

64
Q

Focal segmental glomerulosclerosis (FSGS) is a cause of

A

nephrotic syndrome and chronic kidney disease

65
Q

FSGS generally presents in

A

young adults

66
Q

Causes of FSGS?

A

idiopathic

secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
Alport’s syndrome!

HIV

heroin

sickle-cell

67
Q

Focal segmental glomerulosclerosis is noted for having a high recurrence rate in renal transplants.

A

true

68
Q

Investigations in FSGS?

A

renal biopsy: focal and segmental sclerosis and hyalinosis on light microscopy

effacement of foot processes on electron microscopy

69
Q

Management of FSGS?

A

steroids +/- immunosuppressants

70
Q

Prognosis of FSGS?

A

untreated FSGS has a < 10% chance of spontaneous remission

71
Q

amyloidosis is a term which describes

A

extracellular deposition of an insoluble fibrillar protein termed amyloid
the accumulation of amyloid fibrils leads to tissue/organ dysfunction

72
Q

amyloid is derived from many different precursor proteins

A

true

73
Q

in addition to the fibrillar component, amyloid also contains

A

non-fibrillary protein called amyloid-P component, derived from the acute phase protein serum amyloid P

other non-fibrillary components include apolipoprotein E and heparan sulphate proteoglycans

74
Q

Classification of amyloidosis?

A

systemic or localized
further characterised by precursor protein (e.g. AL in myeloma - A for Amyloid, L for immunoglobulin Light chain fragments)

75
Q

Diagnosis of amyloidosis?

A

Congo red staining: apple-green birefringence
serum amyloid precursor (SAP) scan
biopsy of rectal tissue

76
Q

How often should diabetic patients be screened for renal problems? How is this done?

A

all patients should be screened annually

urinary albumin:creatinine ratio (ACR)
should be an early morning specimen

77
Q

For diabetic nephropathy

ACR > ? = microalbuminuria

A

2.5

78
Q

Management of diabetic nephropathy?

A

dietary protein restriction
tight glycaemic control
BP control
control dyslipidaemia e.g. Statins

79
Q

Aim for BP control in diabetic nephropathy?

A

<130/80mmghg

80
Q

in diabetic nephropathy benefits independent of blood pressure control have been demonstrated for ACE inhibitors (ACE-i) and angiotensin II receptor blockers (A2RB).

A

true

81
Q

Combinations of ACE-i and A2RB are not commonly used anymore following the ON-TARGET trial which showed worse outcomes for patients on dual blockade in diabetic nephropathy

A

true

82
Q

Membranoproliferative glomerulonephritis is also known as

A

mesangiocapillary glomerulonephritis

83
Q

How does Membranoproliferative glomerulonephritis present?

A

nephrotic syndrome, haematuria or proteinuria

84
Q

Prognosis of Membranoproliferative glomerulonephritis

A

poor

85
Q

Which type of Membranoproliferative glomerulonephritis is most common?

A

Type 1

86
Q

What is Type 1 Membranoproliferative glomerulonephritis caused by?

A

cryoglobulinaemia, hepatitis C

87
Q

What is type 2 Membranoproliferative glomerulonephritis caused by?

A 
causes:
 partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face)

factor H deficiency
caused by persistent activation of the alternative complement pathway

88
Q

Type 1 Membranoproliferative glomerulonephritis will show what on renal biopsy?

A

electron microscopy: subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance

89
Q

Type 2 Membranoproliferative glomerulonephritis will have low circulating levels of what? Why is this?

A

C3
C3b nephritic factor is found in 70%
an antibody to alternative-pathway C3 convertase (C3bBb)
stabilizes C3 convertase

90
Q

What will Type 2 Membranoproliferative glomerulonephritis show on biopsy?

A

electron microscopy: intramembranous immune complex deposits with ‘dense deposits’

91
Q

What is T3 Membranoproliferative glomerulonephritis caused by?

A

hepatitis B and C

92
Q

How is Membranoproliferative glomerulonephritis managed?

A

steroids may be effective

93
Q

Post-streptococcal glomerulonephritis typically occurs how long following a group A beta-haemolytic Streptococcus infection

A

7-14 days

94
Q

What is the usual culprit for post strep GN?

A

Streptococcus pyogenes

95
Q

Describe pathophysiology of post strep GN

A

immune complex (IgG, IgM and C3) deposition in the glomeruli

96
Q

Who is most commonly affected by post strep GN

A

children

97
Q

Signs & symptoms of post strep GN?

A

Headache, malaise

Visible haematuria, proteinuria which may result on edema, oliguria

Hypertension

98
Q

What will bloods show in post strep GN?

A

low C3

raised ASO titre

99
Q

Post strep GN has a good prognosis

A

yes

100
Q

Renal biopsy features in Post strep GN

A

post-streptococcal glomerulonephritis causes acute, diffuse proliferative glomerulonephritis
endothelial proliferation with neutrophils

electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits

immunofluorescence: granular or ‘starry sky’ appearance

4th year passmedicine by topic (96 decks)

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