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RB Y2 Renal > GN 2.0 > Flashcards

GN 2.0 Flashcards

1
Q

what is virtually pathognomic of GN in the urine

A

red cell cast

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2
Q

nephritic syndrome

A
  • Syndrome comprising signs of nephritis, presents with haematuria, hypertension and oedema (not as severe as that in nephrotic syndrome)
  • indicative of a proliferative process affecting the endothelial cells
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3
Q

nephrotic syndrome

A
  • 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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4
Q

how does proteinuria affect BP target

A

aim for 120/75 rather than 130/80

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5
Q

what is the most common GN in the developed world

A

IgA nephropathy

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6
Q

IgA nephropathy

A
  • there is raised abnormal IgA, possibly due to infection, which is targeted by the immune system and forms immune complexes (with IgG) which are deposited in mesangial cells
  • They accumulate and cause local immune activation (pro-inflammatory cytokines are released and macrophages arrive) and injury. RBC pass through into urine
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7
Q

which systemic condition does IgA Nephropathy overlap with

A

HSP

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8
Q

typical patient with IgA Nephropathy

A
  • young man with episodic macroscopic haematuria almost immediately after resp/gi infection
  • recovery is rapid between attacks
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9
Q

how soon after infection does IgA Nephropathy tend to occur

A

1-2 days

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10
Q

presentation of IgA Nephropathy

A
  • asymptomatic/intermittent macroscopic/microscopic haematuria ± nephritic syndrome
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11
Q

what is seen on investigation of IgA nephropathy

A
  • LM: diffuse mesangial IgA deposition. Mesangial cell proliferation and expansion
  • IF: immune deposits (IgA and C3) in mesangium
    • The finding of complexes that contain IgA can differentiate it from other GN
  • EM: electron dense deposits in the mesangium
  • normal complement levels
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12
Q

prognosis of IgA nephropathy

A

25% progress to ESRF n ten years

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13
Q

management of IgA nephropathy

A

main focus is preventing further damage and avoiding end stage kidney disease

  • BP control: ACEi and ARBs/fish oil
  • Prevent immune complex formation: corticosteroids
  • With nephritic presentation, immunosuppression may slow down decline of renal function
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14
Q

how does post-streptococcal GN present

A

nephritic syndrome

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15
Q

how common is post-streptococcal

A

very rare IRL

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16
Q

how long after infection does post-streptococcal present

A

few weeks

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17
Q

notifiable biochemical markers in post-streptococcal

A

low complement

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18
Q

what is found in the urine in post-streptococcal

A

proteinuria (even tho it is associated with nephritic syndrome - remember!)

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19
Q

RPGN

A
  • purely a marker of severeity
  • acute deterioration of kidney function, associated with crescent formation
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20
Q

how severe is RPGN

A

can cause ESRF over a few days

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21
Q

causes of RPGN

A

Vasculitis e.g. ANCA+:

  • Pauci-immune (no anti-GBM, no immune complexes)
    • cANCA (GPA) and pANCA (microscopic polyangiitis and eGPA)

Immunological e.g. ANCA-:

  • Anti-GBM: Good pastures disease
  • Immune complex disease: HSP/IgA, SLE, post-streptoccocal glomerulonephritis
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22
Q

how do crescents form

A
  • seen in RPGN and Goodpasture’s
  • 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 ability to filter, can quickly lead to AKI.
  • There is active urinary sediment: RBC, RBC and granular casts
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23
Q

clinical presentation of RPGN

A
  • AKI ± systemic features
  • There is often an insidious onset, with a long history of general malaise
  • General: malaise, fatigue, fevers
  • Skin: cutaneous nodules
  • Neurological: mononeuritis multiplex
  • MSK: myalgia, arthritis
  • Eyes: iritis, uveitis
  • Respiratory: haemoptysis, SOB
  • Other: oral ulceration
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24
Q

what must be done urgently with RPGN

A

renal biopsy

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25
Q

anti-GBM IF

A

linear shape

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26
Q

immune complex deposition on IF

A

granular

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27
Q

treatment of RPGN

A

should be prompt and consist of strong IS with supportive care including dialysis if needed

  • Poor prognosis
  • Anticoagulants to reduce fibrin build up in crescent
  • Aggressive immunosuppression with high-dose IV steroids and cyclophosphamide ± plasma exchange
28
Q

how does Goodpasture’s present

A
  • haematuria ± nephritic syndrome
  • haemoptysis
29
Q

goodpasture’s pathophysiology

A
  • type II hypersensitivity reaction in which anti-GBM antibodies bind to type IV collagen in lungs and kidneys
30
Q

lung involvement in goodpasture’s

A
  • more common in smokers, and it is thought that smoking is a trigger for the disease
  • haemoptysis
31
Q

Goodpasture’s - typical patient age and sex

A

young male

32
Q

which gene is goodpasture’s associated with

33
Q

what is seen on LM of goodpasture’s

A

crescent formation

34
Q

what is seenon IF of goodpasture’s

A

linear IgG deposiiton along basement membrane

35
Q

management of goodpasture’s

A
  • Plasma exchange to remove the circulating antibody
  • Steroids
  • Cyclophosphamide
36
Q

define nephrotic syndrome

A

Defined as proteinuria >3.5g/d, hypoalbuminaemia (<25g/L, usually much lower) and oedema

severe hyperlipidemia

37
Q

why is ​severe hyperlipidemia present in nephrotic syndrome

A

by product of the liver tyring to make more albumin

38
Q

what does ​severe hyperlipidemia caause in nephrotic syndrome

A

procoagulant state, classically renal vein thrombosis

39
Q

how does renal vein thrombosis present

A

flank pain and haematuria, can be a sudden onset

40
Q

features of nephrotic syndrome

A
  • Periorbital oedema is present, often in the morning and drains throughout the day
    • Classically seen in kids
  • followed by full body oedema
  • thrombotic complication may be the first sign
41
Q

what is the most common type in children

A

minimal change

42
Q

incidence of minimal change

A

two peaks - child hood and later on around 60

43
Q

EM of minimal change

A

podocyte apoptosis, loss of gaps between podocytes

44
Q

treatment of minimal change

A
  • steroids, 94% get total remission
  • prednisolone, start at 40-60 mg
  • relapses can occur
45
Q

wha must be given with long term steroid use

A

PPI and bone protection - bisphosphoante

46
Q

how do adults respond to treatment compared o children in minimal change

A

may be slower

47
Q

how is frequently relapsing minimal change disease treated

A

cyclophsophamide or cyclosporin (to reduce steroid dose)

48
Q

prognosisof minimal change

A

good - 1% to ESRF

49
Q

FSGS severity

A

severe, around 50% have impaired renal function

50
Q

causes of FSGS

A
  • May be primary (idiopathic) or secondary (HIV, heroin use (IVDU), sickle cell disease, obesity, reflux)
51
Q

HIV FSGS

A

associated with a collapsing type which has a poorer prognosis

52
Q

treatment of FSGS

A
  • :inconsistent response to steroids (around 30%)
  • cyclophosphamide or cyclosporine are considered if steroid resistant
53
Q

compare the EM in primary and secondary FSGS

A
  • Primary FSGS: diffuse podocyte process fusion
  • Secondary FSGS: podocyte process fusion limited to sclerotic areas
54
Q

causes of membranous nephropathy

A
  • Most idiopathic, but can often secondary to autoantibody generation in response to e.g.
    • malignancy
    • hepatitis B
    • malaria, drugs (gold, penicillamine, NSAIDs)
    • autoimmune diseases (SLE – class V, RA)
55
Q

which type of GN can be caused by malignancy

A

membranous nephropathy - lung, prostate, breast and colon

56
Q

findings on LM of membranous

A
  • immune complex deposition between podocytes and GBM
  • spike and dome pattern
57
Q

which stain is used on LM for membranous

A

special silver stain

58
Q

treatment of membranous

A
  • Underlying cause in secondary
  • In idiopathic treatment involves general measures such as ACEi/ARBs and diuretics
  • In severe cases, steroids, alkylating agents (e.g. cyclophosphamide), B cell monoclonal antibody (Rituximab)
59
Q

prognosis of membranous

A

Rule of thirds

  • 1/3: spontaneous remission
  • 1/3: remain proteinuric
  • 1/3: progress to ESRF
  • Good prognostic features include female sex, young age at presentation and asymptomatic proteinuria of a modest degree at the time of presentation
60
Q

which specific Ab have been found to be associated with membranous nephropathy

A
  • Antibodies directed against phospholipase A2 receptor are found in up to 80% of patients with idiopathic membranous nephropathy
61
Q

membrano-proliferative

A

mixed nephrotic/nephritic syndrome - more varied clinical presentation

62
Q

causes of Membrano-Proliferative

A
  • Idiopathic
  • Autoimmune e.g. SLE, RA
  • Cancer
  • Hepatitis C
63
Q

LM of membrano-proliferative

A

tram track GBM

64
Q

management and prognosis of membrano-prolfierative

A

poor, steroids may be effective

65
Q

low complement GN

A

endocarditis or post streptococcal

RB Y2 Renal (26 decks)

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