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Glomerulonephritis Flashcards

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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
what is the cause of minimal change glomerulonephritis?
idiopathic, associated with Hodkins Lymphoma, NSAIDs, rifampicin, mono
26
what is the pathophysiology of Minimal Change Glomerulonephritis?
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
27
what are the clinical features of minimal change glomerulonephritis?
nephrotic syndrome, normotension, proteinuria
28
what are the histological features of minimal change biopsy?
normal renal biopsy on LM & IF, foot process fusion on EM
29
what is the management of minimal change glomerulonephritis?
oral steroids (94% complete remission), 2nd line = cyclophosphamide, majority reoccur
30
what are the primary causes of focal segmental glomerulosclerosis?
unknown
31
what are the secondary cayses of focal segmental glomeruloscelroiss?
sickle cell, HIV, heroin, kidney hyper fusion, increased pressure in glomerular capillaries, obesity, reflux, renal transplant reoccurrence
32
what is the pathophysiology of focal segmental glomerulosclerosis?
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
what are the clinical features of Focal Segmental Glomerulosclerosis?
nephrotic syndrome
34
what are the histological features of Focal Segmental Glomerulosclerosis?
focal and segmental sclerosis and hylaniosis on LM, minimally on IF, effacement of podocytes on EM
35
what is the management of Focal Segmental Glomerulosclerosis?
Steroids +/- immunosuppressants
36
what is the epidemiology of Membranous Glomerulonephritis?
• Most common type in adults
37
what is the primary cause of Membranous Glomerulonephritis?
idiopathic
38
what are the secondary causes of Membranous Glomerulonephritis?
infections (hep B/parasites), connective tissue disease, cancers, drugs (penicillin’s/gold), malignancy
39
what is the pathophysiology of Membranous Glomerulonephritis?
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
what are the clinical features of Membranous Glomerulonephritis?
2nd most common cause of nephrotic syndrome
41
what is the histological appearance of Membranous Glomerulonephritis?
spike and dome appearance
42
what is the management of Membranous Glomerulonephritis?
ACE/ARB, immunosuppression, anticoagulation
43
what is the prognosis of Membranous Glomerulonephritis?
rule of 1/3 – 1/3 spontaneous remission, remain proteinuria, ESRF
44
what is the immunosuppressive management of Membranous Glomerulonephritis?
steroids/alkylating agents/ B cell monoclonal AB
45
what is membranoproliferative glomerulonephritis also known as?
MESANGIOCAPILLARY GLOMERULONEPHRITIS
46
what is the cause of Type 1 Membranoproliferative glomerulonephritis?
cryoglobinaemia, Hep B, Hep C
47
what is the cause of Type 2 Membranoproliferative glomerulonephritis?
partial lipodystrophy, factor H deficiency
48
what is the cause of Type 3 Membranoproliferative glomerulonephritis?
hep B and C
49
what is the pathophysiology of Type 1 Membranoproliferative glomerulonephritis?
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
what is the pathophysiology of Type 2 Membranoproliferative glomerulonephritis?
dense deposit disease  Nephritic factor (stabilises C3 convertase) – anti C3bBb, C3NeF  Only compliment deposits, no immune complexes  Low circulating levels of C3
51
what is the pathophysiology of Type 3 Membranoproliferative glomerulonephritis?
immune complexes and complement deposit in subepithelial and subendothelial
52
what are the histological features of Type 1 Membranoproliferative glomerulonephritis?
tram track appearance, glomeruli appear granular
53
what are the histological features of Type 2 Membranoproliferative glomerulonephritis?
reduced serum compliment deposits, no immune complexes
54
what are the clinical features of Type 3 Membranoproliferative glomerulonephritis?
nephrotic + nephritic
55
what is the management of Type 3 Membranoproliferative glomerulonephritis?
steroids
56
IgA nephropathy is also known as...
Bergers Disease
57
what is the epidemiology of IgA nephropathy?
• Most common cause of glomerulonephritis
58
what is the cause of IgA nephropathy?
often occur after GI/Resp infection – ½ days | o Associated with: alcoholic cirrhosis, coeliac, Henoch-Schonlein purpura
59
what is the pathophysiology of IgA nephropathy?
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
what are the clinical features of IgA nephropathy?
o Macroscopic haematuria o Asymptomatic microhaematuria +/- non nephrotic range proteinuria o Nephritic syndrome + associated Henock Schoenlein Purpura
61
what are the histological features of IgA nephropathy?
mesangial hypercellularity, positive immunofluorescence for IgA & C3
62
how is IgA nephropathy managed?
BP control/Ace inhibitors & ARBS/ Fish oil
63
what is Henoch-Schonlein Purpura?
Systemic variant of IgA Nephropathy
64
what are the clinical features Henoch-Schonlein Purpura?
Systemic variant of IgA Nephropathy
65
what is post Streptococcal Nephropathy also known as?
Proliferative Glomerulonephritis
66
what is the cause of | Post Streptococcal Nephropathy?
Group A, B-haemolytic streptococci
67
what is the pathophysiology of Post Streptococcal Nephropathy?
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
what are the clinical features of Post Streptococcal Nephropathy?
headaches, malaise, haematuria, proteinuria, hypertension, oliguria, periorbital oedema – NEPHRITIC Syndrome
69
what is the histology of Post Streptococcal Nephropathy?
diffuse proliferative glomerulonephritis, endothelial proliferation with neutrophils, EM shows subepithelial humps, IF granular or starry
70
what are the differences between IgA vs Post Strep
1-2 days vs 1-2 week UTI, young males vs URTI macroscopic haematuria vs proteinuria
71
Rapidly Progressing Crescenteric Glomerulonephritis is known as...
• Most aggressive
72
what is the cause of Type 1 Rapidly Progressing Crescenteric Glomerulonephritis?
anti-GBM – good pastures syndrome
73
what is the cause of Type 2 Rapidly Progressing Crescenteric Glomerulonephritis?
immune complex mediated – post strep, lupus (ANCA +ve or -ve), IgA nephropathy
74
what is the cause of Type 3 Rapidly Progressing Crescenteric Glomerulonephritis?
ANCA (cANCA = Wegners, pANCA = Chung Strauss syndrome)
75
what is the pathophysiology of Rapidly Progressing Crescenteric Glomerulonephritis?
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
what are the clinical features of Rapidly Progressing Crescenteric Glomerulonephritis?
nephritic syndrome, symptoms associated with cause disease, AKI + systemic symptoms, frank haematuria
77
what are the IM features of Rapidly Progressing Crescenteric Glomerulonephritis?
Type 1 = linear Type 2 = granular Type 3 = negative
78
how is Rapidly Progressing Crescenteric Glomerulonephritis managed?
immunosuppressants (steroids = prednisolone, cytotoxic = azathioprine), plasmapheresis
79
what are the additional clinical features of Good Pastures syndrome?
kidney problems then massive pulmonary bleed,

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