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Renal > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What is glomerulonephritis?

A

immune-mediated disease of the kidneys affecting the glomeruli with secondary tubulointerstital amage

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2
Q

What mediates GN?

A

humoral- antibody mediated- intrinsic or planted antigent or deposition of circulating immune complexes

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3
Q

What happens in GN to the glomerular membrane?

A

disruption of the barrier leads to haematuria and/or proteinuria

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4
Q

What happens if there is damage to enothelial or mesangial cells?

A

proliferative lesion and RBCs in the urin

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5
Q

What happens if there is damage to the podocytes?

A

non-proliferative lesion and protein in the urine

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6
Q

Why does damage to different cells at the glomerulus cause different responses?

A

cells of the nephron respond to injury in different ways

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7
Q

What happens to the podocytes when they are injured?

A

atrophy- loss of size/charge specific barrier

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8
Q

What happens if there is injury to the mesangium?

A

mesangial cells proliferate and release ATII and chemokines; attracts inflammatory cells

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9
Q

What happens if there is injury to the endothelial cells?

A

vasculitis

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10
Q

What is the difference between endothelial and mesnagial injury if they are both prolferative lesions?

A

endothelial injury is a much more aggressive process and has lots of inflammation

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11
Q

What is done if there is haematuria seen on urinalysis?

A

RBC (dysmrophic; granular casts and lipiduria

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12
Q

What is done is there is protein seen on UA?

A

PCR

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13
Q

What is the typical presentation of haematuria with GN?

A

asymptomatic microscopic or painless macroscopic

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14
Q

What is microalbuminuria?

A

30-300mg albuminuria/day

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15
Q

What is heavy proteinuria?

A

1-3g/day

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16
Q

What is nephrotic syndrome efined as in proteinuria?

A

> 3g/day

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17
Q

What is the appearance of RBCs on microscopy if they have come from the glomerulus? why?

A

dysmorphic- have been squeezed through the tubule

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18
Q

What are RBC casts?

A

protein that tubules produce gathers roudn the blood cells and they end up in a tubular shaped clump

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19
Q

What is nephritic syndrome?

A

ARF; oliguria; oedema/fluid retention; HT; active urinary sediment

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20
Q

What is active urinary sediment?

A

RBCs; RBC and granular casts

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21
Q

What is nephritic syndrome indicative of?

A

a proliferative process affeting endothelial cells

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22
Q

What is nephrotic syndrome?

A

proteinuria >3g/day; hypoalbuminaemia; oedema; hypercholeseterolaemia

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23
Q

What is nephrotic syndrome indicative of?

A

a non-proliferative process affecting podocytes

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24
Q

What are the complications of nephrotic syndrome?

A

infections; renal vein thrombosis; PE; volume depletion

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25
Q

Why do patients with nephrotic syndrome get infections?

A

loss of opsonising antibodies

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26
Q

What should be suspected with AKI in nephrotic syndrome?

A

renal vein thrombosis

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27
Q

What causes volume depletion with nephrotic syndrome?

A

overagressive use of diuretics

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28
Q

What may volume depletion lead to?

A

pre-renal ARF

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29
Q

What is the difference between interstital nephritis and GN on urinemicroscopy?

A

interstital nephritis doesn’t have dysmorphic RBCs

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30
Q

How are renal biopsies analysed?

A

light microscopy; immunofluorescence; EM

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31
Q

What does diffuse GN indicate?

A

> 50% glomeruli affeced

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32
Q

What does global/segmental GN indicate?

A

whether all or parts of the glomeruli are affected

33
Q

What is crescenteric GN?

A

presence of crescents- epithelial cell extrancapillary (Bowman’s space) proliferation

34
Q

What are the principles of treatmnet of GN?

A

reduce proteinuria; induce remission of nephrotic syndrome; presence longterm renal function

35
Q

What is the target BP for renal patients?

A

<130/80

36
Q

What is the target BP for patients with proteinuria?

A

<120/75

37
Q

What are the non-immunosuppressive treatments for GN?

A

anti-HTs; ACEi; diuretics; statins; anticoag- if albumin <20

38
Q

When is plasmapharesis considered with GN?

A

if very agressive disease due to circulatin antibodies

39
Q

What is the prupose of giving IV immunoglobulin with GN?

A

will attach autoantibodies

40
Q

What is the prupose of monoclonal T or B cell antibodies in GN

A

directed at B cells which produce the autoantibodies

41
Q

What is the treatmnet of nphrotic patients?

A

fluid and salt restrict; diuretics; ACEi; anticoag; IV albumin- only if volume deplete; immunosuppression

42
Q

What is the definition of complete remission of nephrotic syndrome?

A

proteinuria <300mg/day

43
Q

What is the definition of partial remission of nephrotic syndrome?

A

proteinuria <3G/day

44
Q

What are the riks of immunosuppressing a patient who is nephrotic?

A

increased risk of infeciton- do very badly so offload them vefore start immunosuppressives

45
Q

What is the target in minimal change GN?

A

podocyte but specific antigen and antibody unkown

46
Q

What is the commonest cause of nephrotic syndrome in chidlren?

A

minimal change

47
Q

What is seen on EM with minimal change?

A

foot process fusion

48
Q

What is the first line for minimal change?

A

steroids

49
Q

What is second line for minimal change GN?

A

cyclophosphamide

50
Q

What is the prognosis for minimal change?

A

does not cause progressive renal failure

51
Q

What is the commonest cause of nephrotic syndrome in adults?

A

focal segmental glomerulosclerosis

52
Q

What are the secondary causes of FSGS?

A

HIV; heroin use; obesity; reflux nephropathy

53
Q

What is the treatmnet for FSGS?

A

steroids

54
Q

What is the prognosis for FSGS?

A

50% progress to ESRF after 10 years

55
Q

What happens in FSGS?

A

podocyte injury- parietal epithelial cells try to transfer over to atrophied pododcytes to fill hole creating scar tissue

56
Q

What is the second commonest cause of nephrotic syndrome in adults?

A

membranous nephrotpathy

57
Q

What are the important secondary causes of membranous nephropathy?

A

infections- hep B; SLE; malignancies; drugs- gold; pencillamine

58
Q

What is seen on renal biospy with membranous nephropathy?

A

subepithelial immune complex deposition in the BM- thickened basmement membrane

59
Q

What is the prognosis for membranous nephropathy?

A

30% progress to ESRF in 10 years

60
Q

What is the antigen in membranous nephropathy?

A

within podocyte- phosopholipase A2 receptor

61
Q

what is the antibody in membranous nephropathy?

A

anti-PLA2r AB

62
Q

What is the treatment for MN

A

steroids; alkylating agents (cyclophosphamide)

63
Q

What is the presentation of IgA nephropathy?

A

asymptomatic microhaematuria +/- non-nephrotic range proteinuria; or macroscopic haematuria after resp/GI infection; AKI/CKD

64
Q

What vasculitis is IgA nephropathy associated with?

A

Henoch-Schonlein Purpura

65
Q

What are the symtpoms of HSP?

A

arthritis; colitis; purpuric skin rash

66
Q

What is seen on renal biopsy with IgA nephropathy?

A

mesangial cell prliferation and expansion with IgA deposits in mesangium

67
Q

What is the prognosis for IgA nephropathy?

A

25% progress to ESRF in 10-30 years

68
Q

What is the treatment for IgA nephropathy?

A

BP control; ACEi; fish oil

69
Q

What causes IgA nephropathy?

A

antigen is not within kidne- abnormal IgA, IgG is produced against the abnormal IgA whcih get stuck in the mesangium

70
Q

Why is there an exacerbation of IgA nephropathy with infection?

A

infection of mucosal surfaces eg GI or resp- increase in IgA

71
Q

What happens with rapidly progressive glomerulonephritis?

A

rapid deterioration in renal function over days/ weeks

72
Q

What is rapidly progressive glomerulonephritis associated with on biopsy?

A

glomerular crescents

73
Q

What are the 2 main categroeis of RPGN?

A

ANCA positive nad ANCA negative

74
Q

What are the types of ANCA positive RPGN?

A

GPA nad microscopic polyangiitis

75
Q

What are the types of ANCA negative RPGN?

A

Goodpasture’s; HSP; SLE

76
Q

How does ANCA cause a vasculitis?

A

attacks neutrophil cytoplasms which become sticky and bind to vascular walls which begins the inflam cascae and proteolytic enzymes are produces which destroy the vascular wall

77
Q

What happens in RPGN when the BM is interrupted?

A

inflammatory cells and RBCs gather in Bowman’s space in the shape of a crescent which compresses the glomerular tuft and closes the cpiallry lumens leading to glomerular death

78
Q

What is the antigen in Goodpasture’s?

A

type 4 collagen in GBM

79
Q

What are the treatments for RPGN?

A

immunosuppression and plasmapharesis

Renal (33 decks)

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