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Charis & Ellie vs Renal > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

what is glomerulonephritis?

A

immune-mediated diseases of the kidney affecting the glomeruli (characteristically by inflammation)
usually affecting both kidneys
usually occurs several weeks after an infection (secondary to tubulointerstitial damage)

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2
Q

what part of the immune system is involved in glomerulonephritis?

A

humoral - antibody
- intrinsic/ planted antigen
- deposition of circulating immune complexes
T-cell mediated
inflammatory cells, mediators and complements

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3
Q

who gets it?

A

Primary = idiopathic (majority)

Secondary

  • infections
  • drugs
  • associated malignancies
  • part of systemic disease: ANCA +ve, vasculititis SLE, GPA, HSP
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4
Q

How are glomerulonephritis’s classified?

A 
By aetiology - primary/secondary 
histology 
- proliferative/non-proliferative
- focal (<50%)/ diffuse (>50%)
- global (all of glomeruli)/segmental (part of glomeruli)
- cresentic - RPGN
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5
Q

how does glomerulonephritis present?

A 
haematuria - painless 
proteinuria 
impaired renal function 
hypertension 
nephrotic syndrome 
nephritic syndrome
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6
Q

what is haematuria in glomerulonephritis?

A

Aysymptomatic microscopic haematuria

Episodes of painless macroscopic haematuria
urine microscopy
- dysmorphic RBCs (squished)
- red cell cast (=endothelial injury)

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7
Q

how is it diagnosed?

A 
Clinical presentation 
Blood test (ANA, ANCA, anti-GBM testing)
Kidney biopsy (1:400 risk of bleed)
Examination of urine 
- urinalysis - proteinuria/ haematuria
- Urine microscopy - RBC (dysmorphic), RBC casts, lipiduria 
-Urine protein - creatinine ratio/24hr
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8
Q

histological findings of biopsy?

A

light microscopy
- hypercellularity - inflammatory cells and reactive proliferations
- sclerosis
- crescents - this is bad
electron microscopy (see where the deposits are, can look at BM)
- subepithelial
- mesangial
- subendothelial
immunofluorescence (what antibody and distribution - IgM, IgA, IgG)
- IgG - Goodpasture’s

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9
Q

what is the aim of glomerulonephritis treatment?

A

decrease proteinuria
remission of nephrotic syndrome
longterm renal function

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10
Q

what are the immunosuppressive treatments?

A

corticosteroids (prednisolone PO, methylpredisolone IV)
azathioprine
alkylating agents (cyclophosphamide, chlorambucil)
calcineurin inhibitors
mycophenolate mofotil
plasmapheresis
antibodies - IV immunoglobulin, monoclonal T/B antibodies
Goodpastures - cyclophophamide (azathioprine/ MMF maintenance)

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11
Q

what are the non-immunosuppressive treatments?

A 
anti-HTN (target<130/80 if proteinuria <120/75)
ACEi/ARBs 
diuretics 
statins 
anticoagulants/aspirin/antiplatelets 
dialysis 
transplant
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12
Q

how to treat nephrotic patients?

A 
Aim is sustained remission - complete proteinuria <300mg/day and partial proteinuria <3g/day
fluid restriction 
salt restriction 
diuretics 
ACEi/ARBs
anticoagulation?
IV albumin - if V deplete 
immunosuppression
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13
Q

what is minimal change nephropathy?

A

normal renal biopsy on light microscopy

foot process fusion on electron microscopy (podocytes)

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14
Q

who gets minimal change nephropathy?

A

commonest cause of nephrotic syndrome in children

possibly caused by IL-3

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15
Q

what 3 factors are highly suggestive of minimal change neuropathy?

A

response to steroids/immunosuppressives
occurs with Hodgkin’s lymphoma with remission following successful treatment
patients and family have increased incidence of asthma and eczema (remission of the nephrotic syndrome following antigen avoidance)

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16
Q

how is minimal change nephropathy treated?

A

oral steroids - 94% complete remission

if steroid resistant/dependent/multiple relapses - cyclophosphamide/CSA

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17
Q

what is membranous nephropathy?

A

sub epithelial immune complex deposition in the basement membrane - the basement is thicker and the electron dense deposits create a ‘spike and dome’ appearance

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18
Q

what is the pathogenesis in membranous nephropathy?

A

anti-PLA2r antibody id seen in 70%, PLA2r is an antigen on podocytes
Thickened BM - silver staining

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19
Q

who gets membranous nephropathy?

A

2nd most common cause of nephrotic syndrome in adults
primary - idiopathic
secondary
- associated with infections (Hep B, parasites)
- connective tissue diseases (SLE)
- malignancy (carcinoma, lymphoma)
- drugs (gold, penicillin)

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20
Q

what is the prognosis of membranous nephropathy?

A

30% develop ESRT after 10 years

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21
Q

how is membranous nephropathy managed?

A

steroids
alkylating agents
B cell monoclonal antibody

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22
Q

What is focal segmental glomerulosclerosis?

A 
focal <50% of the tissue 
segmental part of the glomeruli 
focal segmental GS on LM 
minimal Ig/complement deposition
because segmental can be missed on biopsys
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23
Q

who gets focal segmental glomerulosclerosis?

A 
commonest cause of nephrotic syndrome in adults 
primary - idiopathic 
secondary
- HIV
- heroin 
- obesity 
- reflux
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24
Q

what is the prognosis of focal segmental glomerulosclerosis?

A

50% develop ESRF after 10 years

25
Q

what is the management of focal segmental glomerulosclerosis?

A

prolonged steroids

remission in 60%

26
Q

how does it present?

A

massive proteinuria
haematuria
hypertension
renal impairment

27
Q

What is membranoproliferative nephropathy?

A

big lobulated hypercellular glomeruli with thick membranes - tram tracks (duplication of BM)

28
Q

who gets membranoproliferative nephropathy?

A

idiopathic
type 2 - infection, lupus, malignancy
adults and children

29
Q

how does membranoproliferative nephropathy present?

A

nephritic/nephrotic syndrome - can be either

30
Q

what is the prognosis of membranoproliferative nephropathy?

A

is dependent on the severity

31
Q

what is IgA nephropathy?

A

mesiangial cell proliferation and expansion on LM and IgA deposits in the mesangium on immunofluorescence
- follows a resp/GI infection by a couple of days

32
Q

who gets IgA nephropathy?

A 
commonest glomerulonephritis 
associated with HSP 
- arthritis
- colitis 
- purpuric rash
33
Q

how does IgA nephropathy present?

A

asymptomatic microhaematuria +/- non-nephrotic proteinuria
macroscopic haematuria after a couple of days resp/GI infection (haematuria a couple of WEEKS after an infection is post-infective nephropathy)
AKI/CKD

34
Q

what is the prognosis of IgA nephropathy?

A

25% develop ESRF after 10 yrs

35
Q

how is IgA nephropathy managed?

A

BP control
ACEi/ARB
fish oil

36
Q

what is rapidly progressive glomerulonephritis?

A

a treatable cause of AKI

it has a systemic association

37
Q

how does rapidly progressive glomerulonephritis present?

A

treatable cause of acute renal failure
rapid deterioration in renal function over days/weeks
active urinary sediment - RBC, RBC and granular cast
part of systemic disease
glomerular crest on biopsy

38
Q

who gets rapidly progressive glomerulonephritis?

A 
ANCA+ve 
- GPA (cANCA, PR3)
- MPA (pANCA, MPO)
- wegners granulomatosis 
- Churg-Strauss syndromes 
ANCA -ve 
- Goodpasture's (antiGBM, IgG)
- HSP/IgA, 
- SLE
39
Q

how is rapidly progressive glomerulonephritis managed?

A

systemic and renal management is needed
immunosuppression
- steroids: PO prednisolone, IV methylprednisolone
- cytotoxics: cyclophosphamide, mycophenolate, azathioprine
supportive treatment (dialysis)
plasmapheresis

40
Q

what is diabetic nephropathy?

A

kidneys initially enlarge and there is hyperfiltration (GFR >150mL/min)

41
Q

pathology in diabetic nephropathy?

A

diffuse and nodular glomerulosclerosis
Kimmel Stiel Wilson lesion - nodules
thickening of glomerular basement membrane and mesangial expansion
also microvascular disease - arterial sclerosis

42
Q

how is diabetic nephropathy managed?

A

lifestyle advice

ACEi/ARB regardless of BP

43
Q

linear IgG glomerularnephritis?

A

Goodpasture’s Syndrome

44
Q

difference between glomerulonephritis and glomerulopathy?

A

if there is predominant inflammation on histology then glomerular disease can be glomerulonephritis
if inflammation is absent - an awful lot of overlap and they are sometimes used interchangeably but this isn’t correct

45
Q

what cells are more involved in nephrotic syndrome?

A

pOdocytes

  • proteinuria
  • oedema
  • hyperlipidaemia
46
Q

what cells are more involved in nephritic?

A

endothelial and mesangial cells

  • haematuria
  • hypertension
47
Q

What is nephritis?

A

Generic term that means inflammatory of kidneys, not a diagnosis or syndrome with criteria

48
Q

What is nephritic syndrome/acute nephritis syndrome?

A

Haematuria
Oliguria
Proteinuria
Fluid retention

49
Q

What is oliguria?

A

Significantly reduced urine output

50
Q

What is nephrotic syndrome?

A

Refers to group of symptoms without specifying underlying cause

-Not a disease, a way of explaining symptoms

Criteria:

  • Peripheral oedema
  • Proteinuria
  • Serum albumin
  • Hypercholesterolaemia
51
Q

Types of glomerular nephritis?

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous glomerulonephritis
  • IgA nephropathy
  • Post-streptococcal glomerulonephritis
  • Mesangiocapillary glomerulonephritis
  • Rapidly progressive glomerulonephritis
  • Good pasture syndrome
52
Q

What is IgA nephropathy AKA?

A

Mesangioproliferative glomerulonephritis

53
Q

What are most types of glomerulonephritis treated with?

A

Immunosuppression (roids)

BP control with ACEis/ARBs

54
Q

Presentation of nephrotic syndrome?

A

Usually oedema
Possible frothy urine
Predisposes patients to thrombosis, HT, and high cholesterol

55
Q

Most common cause of primary glomerulonephritis?

A

IgA nephropathy

56
Q

Most common type of glomerulonephritis overall?

A

Membranous glomerulonephritis

57
Q

what are the nephrotic syndrome triad?

A

proteinuria >3g/day
hypoabuminaemia <30g
oedema (hypercholesterolaemia)

58
Q

what syndrome is often seen with normal renal function?

A 
nephrotic syndrome 
complications 
- infection 
- RV thrombosis 
- PE
59
Q

what are the signs and symptoms of nephritic syndrome?

A 
AKI 
oliguria 
oedema/fluid retention - not to the degree of nephrotic 
hypertension 
active urinary sediment 
- RBC
- granular cast
- proteinuria

Charis & Ellie vs Renal (40 decks)

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