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RB Y2 Renal > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

pathogenesis

A

immunologically mediated disorder

  • humoral - Ab driven
  • cell mediated (T cells)
  • involvement of inflammatory cells, mediators and complements
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2
Q

define

A

immune mediated disorder of the kidneys affecting the glomeruli, with secondary tubulo-interstitial damage

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3
Q

name 3 consequences of inflammation of the glomerulus

A
  • damage to the glomerulus restricts blood flow, leading to compensatory increase in systemic BP
  • damage to the filtration mechanism allows protein and blood to enter the urine
  • loss of the usual filtration capacity leads to AKI
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4
Q

what does damage to endothelial cells lead to

A
  • vasculitis - most aggressive form of inflammation in the kidney, can lead to AKO
  • haematuria
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5
Q

what does damage to mesangial cells lead to

A
  • proliferative lesion, release of angiotensin II which causes vasoconstriction
  • chemokines are released which attract inflammatory cells
  • haematuria
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6
Q

what does damage to podocytes cause

A
  • non-proliferative lesion - podocytes atrophy, lose filtration barrier
  • protein in urine
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7
Q

broad presentation of GN

A
  • specific syndrome eg nephrotic or nephritic
  • blood pressure
  • urine dipstick: protein/blood
  • renal function impairement
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8
Q

compare the presentation of nephritic syndrome to nephrotic

A
  • nephrotic syndrome: Defined as proteinuria >3g/d, hypoalbuminuria (<25g/L) and oedema with severe hyperlipidaemia (and cholesterol). This is indicative of a non-proliferative process affecting podocytes
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9
Q

nephritic syndrome

A

syndrome comprising signs of nephritis, often occurs in GB

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10
Q

aetiology

A
  • the majority are primary with no underlying drive to disease
  • 2y - infections, drugs, autoimmunity, malignancy, systemic disease
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11
Q

define focal and diffuse

A
  • focal <50% glomeruli affected
  • diffuse >50%
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12
Q

define global and segmental

A

all/part of glomerulus affected

focal lesions are often segmental

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13
Q

crescenteric

A

presence of crescents:

  • Glomerular disease leads to gaps or holes in the GBM resulting in epithelial cell proliferation with mononuclear infiltration in Bowman’s space. Ultimately, fibrocellular crescent formation
  • these are associated with RPGN
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14
Q

how does IgA nephropathy present

A
  • macro or microscopic haematuria ± nephritic syndrome
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15
Q

what is the most common GN in the developed world

A

IgA nephropathy

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16
Q

pathology of IgA nephropathy

A
  • there is raised abnormal IgA (possibly due to infection of mucosal membrane)
  • target by the immune system and forms immune complexes with IgG
  • these are deposited in mesangial cells
  • accumulate and cause local immune ativation - proinflammatory cytokine release and macrophages come - and injury
  • RBS pass through into urine
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17
Q

when does IgA nephropathy typically develop

A

during infection of mucosal membrane eg resp/GI tract

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18
Q

how does IgA nephropathy progress

A
  • over time due to glomerular inflammation and injury, patients progress to renal failure
  • 25% progress to ESRF in 10-30 years
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19
Q

describe a typical patient with IgA nephropathy

A
  • Typical patient: young man with episodic macroscopic haematuria after respiratory/G.I. infection, recovery is rapid between attacks
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20
Q

what is IgA Nephropathy associated with systemically

A

Henoch Schonlein purpura

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21
Q

biopsy of IgA Nephropathy

A

mesangial proliferation and expansion

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22
Q

IF and EM of IgA Nephropathy

A

immune deposits (IgA and C3) are seen in mesangium

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23
Q

H&E stain of IgA Nephropathy

A

mesangial cell proliferation and expansion

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24
Q

treatment of IgA Nephropathy

A

the aim is to prevent further damage and avoid ESRF

  • control BP: ACEi/ARB, fish oil
  • prevent immune complex formation: corticosteroids
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25
Q

common features of RPGN

A
  • aggressive, potential to cause ESRF over days
  • severe glomerular injury
  • development of crescent shape
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26
Q

crescent formation

A
  • Glomerular disease leads to gaps or holes in the GBM resulting in epithelial cell proliferation with mononuclear infiltration in Bowman’s space.
  • Ultimately, crescent is replaced by scar tissue
  • lose filtration ability
  • quickly leads to AKI
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27
Q
A

crescent

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28
Q

ANCA positive type of RPGN

A
  • pauci-immune (no anti-GBM or immune complexes)
  • cANCA (GPA) and pANCA (microscopic polyangiitis and eGPA)
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29
Q

ANCA negative RPGN

A
  • anti-GBM eg goodpastures disease
  • immune complex disease: IgA, HSP, post-strep GN
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30
Q

clinical presentation of RPGN

A

AKI ± systemic features

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31
Q

what is seen on IF of RPGN

A
  • Anti-GBM – linear as Ab bind to collagen of GBM
  • Immune complex deposition: granular
  • ANCA – negative on IF (Pauci-immune)
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32
Q

usual age of onset of RPGN

33
Q

treatment of RPGN

A

prompt and supportive, prognosis is poor

  • Anticoagulants to reduce fibrin build up in crescent
  • Aggressive immunosuppression with high-dose IV steroids and cyclophosphamide ± plasma exchange
34
Q

ANCA

A
  • circulate throughout bloodstream and adhere to neutrophils in endothelial cells
  • PR3 and MPO are induced onto the surface of neutrophils when they are primed
  • these promote the inflammatory process and perpetuate the vasculitis process
35
Q

define nephrotic syndrome

A
  • proteinuria >3g/day
  • hypoalbuminuria (<25g/L)
  • oedema

severe hyperlipidaemia (total cholesterol>10mmol/l) is often present

36
Q

why is severe hyperlipidaemia often present in nephrotic syndrome

A
  • may be a by product of the liver trying to produce more albumin
  • often resolves with treatment of the syndrome
  • the liver also produces more clotting factors, meaning the person is in a pro coagulant state - blood hyperviscosity
37
Q

renal function and BP in nephrotic syndrome

A
  • renal function usually normal, normal creatinine
  • BP nomral-mild increase
38
Q

pathophysiology of nephrotic syndrome

A
  • non-proliferative process causing injury to podocytes, whichb atrophy
  • this lets proteins through the barrier
  • proteinuria means there are low protein concentrations in the blood, contributing to reduced oncotic pressure
39
Q

features of nephrotic syndrome

A
  • periorbital oedema followed by full body oedema
    • periorbital oedema drains throughout the day
  • a thrombotic compication (eg DVT, PE) may be the first sign
40
Q

why do you not see peri orbital oedema in patients with oedema 2y to heart failure

A

they cant lie flat due to fluid in lungs etc

41
Q

causes of nephrotic syndrome

A
  • primary due to renal disease (listed further on)
  • secondary to systemic disorders (hepatitis, SLE, paraneoplastic, drug related, diabetic nephropathy)
42
Q

treatment aims of nephrotic syndrome

A
  • reduce oedema
  • reduce proteinuria
  • reduce risk of complications
  • treat underlying cause
    • find and treat underlying infections
    • stop causative drugs
  • immunosuppression

the aim is to induce sustained remission (complete remission: <300mg/day, partial: <3g/day)

43
Q

treatment of nephrotic syndrome: reduce oedema

A
  • high doses of loop diuretics and salt restriction
    • gut oedema may prevent oral absorption so IV is useful
  • fluid restriction to 1l a day
  • IV albumin can be used if volume deplete and diuretics not working
44
Q

treatment of nephrotic syndrome: reduce proteinuria

A

start all patients on a ACEi/ARB

45
Q

treatement of nephrotic syndrome: reduce risk of complications

A
  • anticoagulation
  • statin to reduce cholesterol (although often resolves spontaneously when cause treated)
46
Q

complications of nephrotic syndrome

A
  • infection
  • thromboembolism
  • volume depletion
  • hyperlipidaemia
  • vit D def
  • subclinical hypothyroidism
47
Q

complications of nephrotic syndrome: infection

A

loss of opsonising Ab in urine and IS treatment

48
Q

complications of nephrotic syndrome: thromboembolism

A

patient is in a pro coagulant state due to increased clotting factors and platelet abnormalities

  • renal vein thrombosis
  • PE
  • DVT
49
Q

complications of nephrotic syndrome: volume depletion

A
  • can be due to aggressive use of diuretics, as most of the salt and water is trapped in the tissues and cant move into the vascular space quickly enough to be removed
  • patient can be oedematous and volume depleted
50
Q

complications of nephrotic syndrome: vit D deficiency

A
  • 25OH vitamin D is lost in the urine
51
Q

complications of nephrotic syndrome: subclinical hypothyroidism

A
  • normal T3/4 and high TSH
  • due to increasd urinary excretion of thyroid hormones
  • if there is already a low thyroid reserve, the transition into overt hypothyroidism is inevitable
52
Q

nephrotic syndrome: minimal change disease

cause

A
  • idiopathic
  • associated with drugs eg NSAIDs, or paraneoplastic
53
Q

what is the most common cause of nephrotic syndrome in children

A

minimal change disease

54
Q

nephrotic syndrome: minimal change disease

pathophysiology

A
  • cytokine damage to podocyte foot processes
    • IL-13 may be implicated
  • the flatten out
  • negative charge barrier is lost
  • albumin passess through
  • selective proteinuria (some larger proteins still cant pass through)
55
Q

nephrotic syndrome: minimal change disease

biopsy

A
  • normal under light microscopy
  • IF usually negative as there are no immune complexes
  • EM shows fusion of foot processes of podocytes
56
Q

nephrotic syndrome: minimal change disease

treatment

A
  • 94% experience total remission with oral steroids
    • adults respond slower than children
  • some are steroid resistant or have multiple relapses
57
Q

nephrotic syndrome: minimal change disease

how is frequently relapsing or steroid-dependent disease treated

A

cyclophosphamide or ciclosporin

58
Q

prognosis of nephrotic syndrome: minimal change disease

A

1% progress to ESRF

59
Q
A

nephrotic syndrome: minimal change disease

60
Q

what is the most common cause of nephrotic syndrome in adults

61
Q

nephrotic syndrome: FSGS

causes

A
  • primary (idiopathic)
  • 2y - HIV, heroin use, sickle cell disease, obesity, reflux)
62
Q

nephrotic syndrome: FSGS

pathophysiology

A
  • podocytes are damaged and let plasma proteins and lipids through
  • some of these are trapped and build up in the glomerulus
  • these areas develop focal sclerosis
63
Q

nephrotic syndrome: FSGS

presentation

A

usually nephrotic syndrome or proteinuria

around half have impaired rnenal function

64
Q

nephrotic syndrome: FSGS

biopsy

A

segmental sclerosis of some glomeruli

65
Q

nephrotic syndrome: FSGS

EM

A

effacement of some podocyte foot processes

66
Q

nephrotic syndrome: FSGS

IF

A

there may be IgM and C3 (complement) deposits in affected areas

67
Q

nephrotic syndrome: FSGS

treatment

A
  • there is an inconsistent response to steroids (around 30%)
  • cyclophosphamide or ciclopsorin are considered if steroid resistant
68
Q

nephrotic syndrome: FSGS

prognosis

A

partially due to the inconsistent repsonse to steroids, and progressive sclerosis of glomeruli, around 50% progress to ESRF in ten years

69
Q

what is the 2nd most common cause of nephrotic syndrome in adults

A

nephrotic syndrome: membranous nephropathy

70
Q

nephrotic syndrome: membranous nephropathy

causes

A
  • primary - idiopathic
  • 2y to autoantibody generation in response to e.g. malignancy, hepatitis B, drugs (gold, pencillamine), connective tissue diseases (lupus)
71
Q

nephrotic syndrome: membranous nephropathy

pathophysiology

A
  • basement membrane damaged by subepithelial immune complex deposits
  • activate complement system and attract inflammatory cells
  • damaged GBM is leaky - thickened in a spike and dome pattern
72
Q

nephrotic syndrome: membranous nephropathy

biopsy

A

diffusely thickened GBM

73
Q

nephrotic syndrome: membranous nephropathy

IF

A

immune complex deposition in subepithelial area - IgG and C3

granular appearance

74
Q

nephrotic syndrome: membranous nephropathy

treatment

A
  • underyling cause in secondary
  • in primary, general measures eg blood pressure and diuretics
  • steroids, alkylating agents, B cell monoclonal Ab
75
Q

nephrotic syndrome: membranous nephropathy

prognosis

A

30% progress to ESRF in ten years

76
Q

which antibodies are found in around 80% of idiopathic membranous nephropathy

A

phospholipase A2 receptor antibodies

77
Q

clinical presentation of Goodpasture’s disease

A
  • haemoptysis and haematuria
78
Q

good pasture’s disease

A
  • anti-GBM disease
  • autoimmune diseas primarily affecting the lungs and kidney, where the BM are made up of type IV collagen
  • type II hypersensitivity reaction
  • auto-antibodioes bind to type IV collagen and activate the complement system
79
Q

risk factors for Good pasture’s disease

A

genetic, infection, smoking, oxidative stress

RB Y2 Renal (26 decks)

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