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Renal > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

what is glomerulonephritis?

A

Immune mediated disease of the kidneys affecting the glomeruli

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2
Q

what is the summary pathophysiology of the glomerulonephritis?

A
  1. Damage to the glomerulus restricts blood flow, leading to compensatory raised BP
  2. Damage to the filtration mechanism allows protein and blood to enter the urine
  3. Loss of the usual filtration capacity leads to acute kidney injury
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3
Q

what are the types of primary glomerulonephritis?

A 
o	Minimal change
o	FSG
o	Membranous
o	IgA neuropathy
o	Membranoproliferative
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4
Q

what are the causes of secondary glomerulonephritis?

A

caused by infections of drugs, associated with malignancy, or part of systemic disease

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5
Q

what are the histological classifications of glomerulonephritis?

A
  • Proliferative or non-proliferative
  • Focal/diffuse
  • Global/segmental
  • Crescenteric
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6
Q

what are the common clinical features of GN?

A
  • Haematuria
  • Proteinuria
  • Impaired renal function – AKI, CKD, ESRD
  • Nephritic or Nephrotic
  • Weakness, fatigue, anorexia, nausea, vomting, abdo pain, joint pain
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7
Q

what are the two types of treatment for GN?

A

non-immunosuppressive

Immunosuppression

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8
Q

what are the features of non-immunosuppressive management of GN?

A

o Anti-hypertensives (target <130/80,

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9
Q

what are the changes to BP in nephrotic syndrome?

A

Normal-mildly ↑

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10
Q

what are the changes to BP in nephritic syndrome?

A

Moderate-severely ↑

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11
Q

what are the changes to urine in Nephrotic syndrome?

A

Proteinuria > 3.5g/dy

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12
Q

what are the changes to urine in Nephritic syndrome?

A

Haematuria (mild-macro)

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13
Q

what are the changes to GFR in nephrotic syndrome?

A

Normal-mild ↓

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14
Q

what are the changes to GFR in nephritic syndrome?

A

Moderate-severe ↓

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15
Q

what are the primary causes of nephrotic syndrome?

A

minimal change disease, focal segmental glomerulonephritis, membranous glomerulonephritis, membranoproliferative glomerulonephritis, rapidly progressing glomerulonephritis

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16
Q

what are the secondary causes of nephrotic syndrome?

A

diabetic nephropathy, SLE, sarcoidosis, syphilis, Hep B, Sjogren’s Syndrome, HIV, amyloidosis, Multiple myeloma, vasculitis, cancer, congenital nephrotic syndrome, drugs (penicillin)

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17
Q

what is the pathophysiology of Nephrotic Syndrome?

A
  • Effects podocytes
  • Indicates non-proliferative process
  • Allows proteins to pass into urine
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18
Q

what are the mechanisms of proteinuria in nephrotic syndrome?

A

o In response to hyperlipidaemia
o >oncotic pressure – osmotic drive
o Damage causes < permeability

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19
Q

what are the clinical features of nephrotic syndrome?

A
  • Proteinuria>3g/day (mostly albumin, also globulins)

* Hypalbuminaemia (<30), oedema, hypercholesterolaemia, normal renal function, hyperlipidaemia, lipiduria

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20
Q

what are the complications ofnephrotic syndrome?

A

infections, renal vein thrombosis, PE, volume depletion

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21
Q

what is the management of nephrotic syndrome?

A

General – fluid restriction, salt restriction, diuretics, ACE/ARBs, anticoagulation, IV albumin
Immunosuppression

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22
Q

what are the causes of nephritic syndrome?

A
  • IgA neuropathy
  • Mesangiocapillary
  • Post streptococcal glomerulonephritis
  • Rapidly progressive glomerulonephritis
  • Vasculaitis, SLE, cryralbuminaemia
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23
Q

what is the pathophysiology of nephritic syndrome?

A
  • Affecting endothelial cells
  • Indicative of a proliferative process
  • Damage done by antibody/antigen complex – urinary casts formed
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24
Q

what are the clinical features of nephritic syndrome?

A

acute renal failure, oliguria, oedema, hypertension, active urinary sediment – RBCs, RBC and Granular cells = HAEMATURIA + PROTEINURIA

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25
Q

what is the cause of minimal change glomerulonephritis?

A

idiopathic, associated with Hodkins Lymphoma, NSAIDs, rifampicin, mono

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26
Q

what is the pathophysiology of Minimal Change Glomerulonephritis?

A

T cells release cytokines (IL-13) that target and damage podocytes – makes them flatter = effacement. Results in loss of charge barrier. Albumin can pass through but not larger proteins

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27
Q

what are the clinical features of minimal change glomerulonephritis?

A

nephrotic syndrome, normotension, proteinuria

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28
Q

what are the histological features of minimal change biopsy?

A

normal renal biopsy on LM & IF, foot process fusion on EM

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29
Q

what is the management of minimal change glomerulonephritis?

A

oral steroids (94% complete remission), 2nd line = cyclophosphamide, majority reoccur

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30
Q

what are the primary causes of focal segmental glomerulosclerosis?

A

unknown

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31
Q

what are the secondary cayses of focal segmental glomeruloscelroiss?

A

sickle cell, HIV, heroin, kidney hyper fusion, increased pressure in glomerular capillaries, obesity, reflux, renal transplant reoccurrence

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32
Q

what is the pathophysiology of focal segmental glomerulosclerosis?

A

podocytes are damaged allowing plasma and proteins to enter glomerulus, overtime can become trapped and build up in glomerulus = hyalinises, can progress to sclerosis – only occurs in part of and some of glomeruli

33
Q

what are the clinical features of Focal Segmental Glomerulosclerosis?

A

nephrotic syndrome

34
Q

what are the histological features of Focal Segmental Glomerulosclerosis?

A

focal and segmental sclerosis and hylaniosis on LM, minimally on IF, effacement of podocytes on EM

35
Q

what is the management of Focal Segmental Glomerulosclerosis?

A

Steroids +/- immunosuppressants

36
Q

what is the epidemiology of Membranous Glomerulonephritis?

A

• Most common type in adults

37
Q

what is the primary cause of Membranous Glomerulonephritis?

A

idiopathic

38
Q

what are the secondary causes of Membranous Glomerulonephritis?

A

infections (hep B/parasites), connective tissue disease, cancers, drugs (penicillin’s/gold), malignancy

39
Q

what is the pathophysiology of Membranous Glomerulonephritis?

A

o Autoantibodies targeting GBM (Anti-PLA2r antibody) form immune complexes and deposit in sub epithelial space
o Activates compliment system – membrane attack complex attacks podocytes and mesangial cells = become more permeable (proteins enter)
o Over time GBM matrix is deposited between complexes = thickening

40
Q

what are the clinical features of Membranous Glomerulonephritis?

A

2nd most common cause of nephrotic syndrome

41
Q

what is the histological appearance of Membranous Glomerulonephritis?

A

spike and dome appearance

42
Q

what is the management of Membranous Glomerulonephritis?

A

ACE/ARB, immunosuppression, anticoagulation

43
Q

what is the prognosis of Membranous Glomerulonephritis?

A

rule of 1/3 – 1/3 spontaneous remission, remain proteinuria, ESRF

44
Q

what is the immunosuppressive management of Membranous Glomerulonephritis?

A

steroids/alkylating agents/ B cell monoclonal AB

45
Q

what is membranoproliferative glomerulonephritis also known as?

A

MESANGIOCAPILLARY GLOMERULONEPHRITIS

46
Q

what is the cause of Type 1 Membranoproliferative glomerulonephritis?

A

cryoglobinaemia, Hep B, Hep C

47
Q

what is the cause of Type 2 Membranoproliferative glomerulonephritis?

A

partial lipodystrophy, factor H deficiency

48
Q

what is the cause of Type 3 Membranoproliferative glomerulonephritis?

A

hep B and C

49
Q

what is the pathophysiology of Type 1 Membranoproliferative glomerulonephritis?

A

Immune complex deposition from chronic infection or mutation of antibody against complement system proteins
C3 convertase enzyme binds to IgG
 Release oxidants + proteases causing damage of endothelium, thickening of B

50
Q

what is the pathophysiology of Type 2 Membranoproliferative glomerulonephritis?

A

dense deposit disease
 Nephritic factor (stabilises C3 convertase) – anti C3bBb, C3NeF
 Only compliment deposits, no immune complexes
 Low circulating levels of C3

51
Q

what is the pathophysiology of Type 3 Membranoproliferative glomerulonephritis?

A

immune complexes and complement deposit in subepithelial and subendothelial

52
Q

what are the histological features of Type 1 Membranoproliferative glomerulonephritis?

A

tram track appearance, glomeruli appear granular

53
Q

what are the histological features of Type 2 Membranoproliferative glomerulonephritis?

A

reduced serum compliment deposits, no immune complexes

54
Q

what are the clinical features of Type 3 Membranoproliferative glomerulonephritis?

A

nephrotic + nephritic

55
Q

what is the management of Type 3 Membranoproliferative glomerulonephritis?

A

steroids

56
Q

IgA nephropathy is also known as…

A

Bergers Disease

57
Q

what is the epidemiology of IgA nephropathy?

A

• Most common cause of glomerulonephritis

58
Q

what is the cause of IgA nephropathy?

A

often occur after GI/Resp infection – ½ days

o Associated with: alcoholic cirrhosis, coeliac, Henoch-Schonlein purpura

59
Q

what is the pathophysiology of IgA nephropathy?

A

o Abnormal glycosylation of IgA1 antibodies
o Body also recognises them as non-self-produce IgG (anti-IgA1) that form complexes that deposit in mesangial
o Causes complement activation, cytokine release, macrophage mutation
o Also causes mesangial proliferation, glomerular sclerosis, interstitial fibrosis

60
Q

what are the clinical features of IgA nephropathy?

A

o Macroscopic haematuria
o Asymptomatic microhaematuria +/- non nephrotic range proteinuria
o Nephritic syndrome + associated Henock Schoenlein Purpura

61
Q

what are the histological features of IgA nephropathy?

A

mesangial hypercellularity, positive immunofluorescence for IgA & C3

62
Q

how is IgA nephropathy managed?

A

BP control/Ace inhibitors & ARBS/ Fish oil

63
Q

what is Henoch-Schonlein Purpura?

A

Systemic variant of IgA Nephropathy

64
Q

what are the clinical features Henoch-Schonlein Purpura?

A

Systemic variant of IgA Nephropathy

65
Q

what is post Streptococcal Nephropathy also known as?

A

Proliferative Glomerulonephritis

66
Q

what is the cause of

Post Streptococcal Nephropathy?

A

Group A, B-haemolytic streptococci

67
Q

what is the pathophysiology of Post Streptococcal Nephropathy?

A

o Immune complexes of antigen + IgG/IgM form + travel to glomerulus or antigen travels to glomerulus and complexes form there
o Affects BM (subepithelial layer)
o Activation of C3 complement, cytokines, oxidates, proteases causing damage to podocytes – all proteins + red blood cells pass through

68
Q

what are the clinical features of Post Streptococcal Nephropathy?

A

headaches, malaise, haematuria, proteinuria, hypertension, oliguria, periorbital oedema – NEPHRITIC Syndrome

69
Q

what is the histology of Post Streptococcal Nephropathy?

A

diffuse proliferative glomerulonephritis, endothelial proliferation with neutrophils, EM shows subepithelial humps, IF granular or starry

70
Q

what are the differences between IgA vs Post Strep

A

1-2 days vs 1-2 week
UTI, young males vs URTI
macroscopic haematuria vs proteinuria

71
Q

Rapidly Progressing Crescenteric Glomerulonephritis is known as…

A

• Most aggressive

72
Q

what is the cause of Type 1 Rapidly Progressing Crescenteric Glomerulonephritis?

A

anti-GBM – good pastures syndrome

73
Q

what is the cause of Type 2 Rapidly Progressing Crescenteric Glomerulonephritis?

A

immune complex mediated – post strep, lupus (ANCA +ve or -ve), IgA nephropathy

74
Q

what is the cause of Type 3 Rapidly Progressing Crescenteric Glomerulonephritis?

A

ANCA (cANCA = Wegners, pANCA = Chung Strauss syndrome)

75
Q

what is the pathophysiology of Rapidly Progressing Crescenteric Glomerulonephritis?

A

o Inflame mediators, C3b, fibrin pass into Bowmans space as well as macrophages + monocytes and parietal epithelial cells
o Proliferation leads to expansion of epithelial layer into thick crescent shape – scarring + sclerosis, glomerular damage = reduced GFR

76
Q

what are the clinical features of Rapidly Progressing Crescenteric Glomerulonephritis?

A

nephritic syndrome, symptoms associated with cause disease, AKI + systemic symptoms, frank haematuria

77
Q

what are the IM features of Rapidly Progressing Crescenteric Glomerulonephritis?

A

Type 1 = linear
Type 2 = granular
Type 3 = negative

78
Q

how is Rapidly Progressing Crescenteric Glomerulonephritis managed?

A

immunosuppressants (steroids = prednisolone, cytotoxic = azathioprine), plasmapheresis

79
Q

what are the additional clinical features of Good Pastures syndrome?

A

kidney problems then massive pulmonary bleed,

Renal (7 decks)

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