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Renal > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What are features of nephritic syndrome?

A 
Haematuria
Dysmorphic red cells
Red cell casts
Hypertension
Renal failure
Pyuria
Proteinuria
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2
Q

What are the classes of lupus nephritis

A 
1 - minimal mesangial
2 - mesangial proliferation
3 - focal nephritis
4 - diffuse nephritis
5 - membranous nephritis
6 - sclerotic nephritis
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3
Q

What is a RPGN

A

Nephritic syndrome with rapidly progressive renal failure

Pathological equivalent is crescents

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4
Q

What are the 3 groupings of causes of RPGN

A

Immune complex mediated
Pauci-immune
Anti-GBM

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5
Q

What infections typically cause a PIGN (post infectious)

A 
Strep pyogenes (impetigo, pharyngitis)
Staph aureus
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6
Q

What is the time frame from infection to developing PIGN

A

Impetigo 2-6 weeks

Pharyngitis 1-3 weeks

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7
Q

What is the age distribution of anti-gbm disease

A

Males 20-30 - worse prognosis

age greater then 50 - females greater then males, don’t often present with good pastures

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8
Q

Pathology of anti-GBM disease

A

Auto-antibodies against collagen 4 (alpha 3 chain) in the basement membrane, usually IgG

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9
Q

Tests in post infectious GN

A

Low C3, normal C4
Test for strep (culture, ASOT, anti-DNase)
Rarely requires biopsy for diagnosis

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10
Q

Biopsy findings in post-infectious GN

A

Hypercellularity of mesangial and endothelial cells with neutrophil infiltrates
Sub epithelial humps, sub endothelial immune deposits of IgG, IgM, C3

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11
Q

How many of those with anti-GBM have goodpastures

A

30-40%

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12
Q

Treatment of anti-GBM

A

Daily plasmapheresis for 2-3 weeks

Oral steroids and cyclophosphamide

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13
Q

What are features of a nephrotic syndrome

A 
Proteinuria (greater then 3.5g per 24hours)
Hypoalbuminaemia
Hypertension
High cholesterol and lipiduria
Hypercoagulable
Odema/anasarca
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14
Q

Immunofluorescence findings in anti-GBM disease

A

Linear IgG deposition along basement membrane

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15
Q

Treatment of post infectious GN

A

Supportive, minimal need for immunosuppressive even with crescents
May need dialysis
Treat HTN and odema (ACE-I, dieretics)
Treat infection

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16
Q

Who does IgA typically occur in

A

Males, 20-30 years
White/Asians
Most common GN worldwide

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17
Q

Clinical presentation of IgA disease

A
  1. Recurrent episodes of macroscopic haematuria during or immediately after URTI
  2. Persistent asymptomatic microscopic haematuria
  3. RPGN with ARF
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18
Q

Treatment of IgA GN

A

Mild - ACEI

RPGN - steroids, immunosuppression, plasmapheresis

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19
Q

Biopsy findings in IgA

A

Immune complex deposition with mesangial IgA deposits

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20
Q

What are the two types of ANCA and what do they stain against?

A 
cANCA = cytoplasmic staining, typically against proteinase 3 (PR3)
pANCA = peri nuclear staining, typically against myeloperoxidase (MPO)
21
Q

What are clinical features of granulomatosis with polyangitis?

A

Fever, polyarthralgia
Sinusitis, rhinorrhoea, nasal ulcers, saddle nose deformity due to polychondritis
Cough, haemoptysis, SOB
Microscopic haematuria, proteinuria, RPGN
Pupura
Mono neuritis multiplex

22
Q

What small vessel vasculitis is associated with c-anca

A

Granulomatosis with polyangiitis

23
Q

What small vessel vasculitis is associated with p-anca

A

Microscopic polyangiitis

Churg-Strauss is also associated with p-anca

24
Q

What are the 2 classifications of membranoproliferative GN

A

1) Immune complex deposition
- caused by chronic infections, monoclonal gammopathy, autoimmune diseases
2) complement mediated
- caused by either dense deposit disease or c3 glomerulopathy

25
Q

What is the pathogenesis of dense deposit disease

A

C3 nephritic factors which are anti-bodies which stabilise C3 convertase leading to continuous MAC complex formation

26
Q

What is cryoglobulinaemia

A

Immunoglobulins that precipitate in the cold causing deposition of antigen-antibody complexes in small arterioles

27
Q

What are the 3 types of cryoglobulinaemia

A

Type 1
Monoclonal IgM or IgG often due to multiple myeloma or waldenstroms
Type 2
Polyclonal IgG and monoclonal IgM RF against IgG
Often due to Hep b or c and EBV
Type 3
Polyclonal IgG and IgM RF
Due to SLE, sjogrens, lymphoproliferative malignancies and hep c

28
Q

What are some clinical features of cryglobulinaemia

A

Palpable purpura, renal disease (usually MPGN), arthralgias, peripheral neuropathy, low complement

29
Q

What are some causes of minimal change

A

Most common primary

Secondary: NSAIDs, allergies, Hodgkin’s disease

30
Q

What are the biopsy findings in minimal change?

A

No findings on light microscopy or IF

EM shows effacement of podocyte foot processes

31
Q

Clinical features of minimal change

A 
Abrupt onset severe odema (average protein excretion greater then 10g/24hours)
Hypoalbuminaemia
Hypertension
Microscopic haematuria
Lipiduria
32
Q

Treatment of minimal change

A

Steroids
- if adults are resistant to steroids consider doing a biopsy to look for FSGS

Other options: cyclophosphamide, mycophenolate

Adults respond less well to treatment, freq relapses

33
Q

Epidemiology of FSGS

A

Ages 20-40
More common in African Americans
1/3 of nephrotic syndrome in adults

34
Q

Causes of FSGS

A

Primary
Secondary - HIV, hep b, parvovirus, HTN, reflux nephropathy, cholesterol emboli, analgesics, pamidronate, alports, sickle cell, lymphoma

35
Q

Pathology of FSGS

A

Segmental areas of mesangial collapse and sclerosis
Negative IF
Effacement of foot processes on EM

36
Q

Clinical presentation of FSGS

A

Primary presents with nephrotic syndrome

Secondary presents less floridly - non nephrotic proteinuria, renal insufficiency

37
Q

Treatment of FSGS

A

ACE-I
Treat underlying cause
Can trial steroids in primary

  • recurs in grafts after transplant in 25-40%
38
Q

Epidemiology of membranous nephropathy

A

30% of nephrotic syndrome in adults
More common in males (2:1)
Peak incidence 30-50

Idiopathic MN more common in white males over 59
MN in young females should raise suspicion for SLE

39
Q

Causes of membranouse nephropathy

A

70% idiopathic
Secondary
- malignancy (breast, lung, colon,prostate)
- infection (Hep b, malaria, schistomasis)
- rheumatologic (SLE)

40
Q

Pathology of membranous nephropathy

A

LM - thickening of basement membrane
IF - granular deposits of IgG and C3
EM - sub epithelial deposits, spikes ( expansion of GBM between sub epithelial deposits)

41
Q

Progression of membranous nephropathy

A

1/3 spontaneously improve
1/3 remain stable
1/3 progress to ESRF

42
Q

Treatment of membranous nephropathy

A

Immunosuppression in primary (steroids plus cyclophosphamide or Cyclosporin)
Ace-I if persistent proteinuria

  • membranous has the highest rate of renal vein thrombosis, PE, DVT of all nephrotic syndrome
43
Q

What are the four stages of diabetic nephropathy?

A 
1 - hyperfiltration (first 5 years)
2 - microalbuminuric (30-300mg/24h) 
3 - overt proteinuria (>300mg/24h)
4 - nephrotic syndrome, decreasing GFR
5 - ESRF ( 20-30 years)
44
Q

Pathology of diabetic nephropathy

A

Thickening of BM
Negatively charged filtration barrier allows filtration of negatively charged albumin
Expansion of mesangium
Mesangial sclerosis
Hypertensive and hyaline arteriosclerosis

45
Q

What are 3 types of glomerular deposition diseases

A

Light chain deposition disease (myeloma)
Renal amyloidosis
Fibrillary immunotactoid glomerulopathy

46
Q

What is alports syndrome

A

X-linked mutation of alpha-5 chain of collagen type 4

Presentation with deafness, mild proteinuria, haematuria, lenticonus

47
Q

What is thin basement membrane disease

A

Persistent recurrent haematuria without proteinuria/HTN/renal impairment or systemic disease
Benign
Often familial

48
Q

What are the thrombotic microangiopathies?

A

TTP
- reduced ADAMTS13 activity resulting in ultra-large Von willibrand multimers that promote thrombosis

HUS
- caused by enteropathogens that release shiga toxins, which bind causing activation of platelets and thrombosis

Renal (8 decks)

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