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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
What is the pathogenesis of dense deposit disease
C3 nephritic factors which are anti-bodies which stabilise C3 convertase leading to continuous MAC complex formation
26
What is cryoglobulinaemia
Immunoglobulins that precipitate in the cold causing deposition of antigen-antibody complexes in small arterioles
27
What are the 3 types of cryoglobulinaemia
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
What are some clinical features of cryglobulinaemia
Palpable purpura, renal disease (usually MPGN), arthralgias, peripheral neuropathy, low complement
29
What are some causes of minimal change
Most common primary | Secondary: NSAIDs, allergies, Hodgkin's disease
30
What are the biopsy findings in minimal change?
No findings on light microscopy or IF | EM shows effacement of podocyte foot processes
31
Clinical features of minimal change
``` Abrupt onset severe odema (average protein excretion greater then 10g/24hours) Hypoalbuminaemia Hypertension Microscopic haematuria Lipiduria ```
32
Treatment of minimal change
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
Epidemiology of FSGS
Ages 20-40 More common in African Americans 1/3 of nephrotic syndrome in adults
34
Causes of FSGS
Primary Secondary - HIV, hep b, parvovirus, HTN, reflux nephropathy, cholesterol emboli, analgesics, pamidronate, alports, sickle cell, lymphoma
35
Pathology of FSGS
Segmental areas of mesangial collapse and sclerosis Negative IF Effacement of foot processes on EM
36
Clinical presentation of FSGS
Primary presents with nephrotic syndrome | Secondary presents less floridly - non nephrotic proteinuria, renal insufficiency
37
Treatment of FSGS
ACE-I Treat underlying cause Can trial steroids in primary * recurs in grafts after transplant in 25-40%
38
Epidemiology of membranous nephropathy
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
Causes of membranouse nephropathy
70% idiopathic Secondary - malignancy (breast, lung, colon,prostate) - infection (Hep b, malaria, schistomasis) - rheumatologic (SLE)
40
Pathology of membranous nephropathy
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
Progression of membranous nephropathy
1/3 spontaneously improve 1/3 remain stable 1/3 progress to ESRF
42
Treatment of membranous nephropathy
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
What are the four stages of diabetic nephropathy?
``` 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
Pathology of diabetic nephropathy
Thickening of BM Negatively charged filtration barrier allows filtration of negatively charged albumin Expansion of mesangium Mesangial sclerosis Hypertensive and hyaline arteriosclerosis
45
What are 3 types of glomerular deposition diseases
Light chain deposition disease (myeloma) Renal amyloidosis Fibrillary immunotactoid glomerulopathy
46
What is alports syndrome
X-linked mutation of alpha-5 chain of collagen type 4 | Presentation with deafness, mild proteinuria, haematuria, lenticonus
47
What is thin basement membrane disease
Persistent recurrent haematuria without proteinuria/HTN/renal impairment or systemic disease Benign Often familial
48
What are the thrombotic microangiopathies?
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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