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Glomerulonephritis Flashcards

1
Q

What is glomerulonephritis

A

is a renal disease
characterised by inflammation and damage to the
glomeruli.

The ‘glomerulopathies’ are a constellation of diseases
characterised by injury to renal glomeruli.

This glomerular damage allows protein (with or
without blood) to leak into the urine (proteinuria
and haematuria respectively).

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2
Q

What layers make up the filtration barrier

A

Endothelium - capillary wall
Basement membrane - selective barrier to macromolecules
Foot processes podocytes (specialised epithelial cells)

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3
Q

Secondary causes glomerulonephritis

A

Vasculitis (ANCA-ass vasculitis)
Amyloidosis
Diabetes mellitus

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3
Q

Primary causes of glomerulonephritis

A

IgA nephropathy
Minimal change disease
Focal segmental glomerulosclerosis

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4
Q

Focal vs diffuse glomerulopathy

A

50% cut off - number of glomeruli affected

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5
Q

Global vs segmental glomerulopathy

A

50% of glomerulus itself is cut off

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6
Q

Immune mediated glomerulus damage

A

Immune complex deposition
activate pro inflam and complement response
Circulating anitbodies target key basement membrane proteins or endothelial cells -> inflammatory reaction

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7
Q

Non immune damage to glomeruli mechanism

A

Structure and/or function of podocytes affected disrupt filtration barrier -> larger macromolecules leak through
OR
accumulation of non immune material -> dysgunction

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8
Q

Histological patterns

A

Proliferative - increased cells + inflam response
Non proliferative - structural - sclerosis
Crescents - extracapillary lesions in bowmans capsule due to immune cell accumulartion = severe injury to capillary wall

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9
Q

What glomerulonephrotic diseases are proliferative

A

Glomerular inflammation with haematuria +/- nephritic syndrome

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10
Q

what glomerulopathies are non proliferative

A

Excess protein loss and nephrotic syndrome

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11
Q

Groups of glomerulopathies

A

Isolated haematuria
Isolated proteinuria
Nephrotic syndrome
Nephritic syndrome
Rapidly progressive glomerulonephritis

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11
Q

What is a crescent

A

extracapillary lesions in Bowan’s capsule
due to accumulation of immune cells, fibroblasts,
epithelial cels and fibrin. Crescents represent
severe injury to the capillary wall that results in
glomerular membrane rupture.

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12
Q

What is isolated haematuria

A

Persistent haematuria in absence of proteinuria and normal renal function
Reassess over 1-4 weeks to determine

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12
Q

Causes of isolated haematuria

A

IgA nephropathy
Alport syndrome
Thin basement membrane disease
Exclude non renal causes

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13
Q

What causes isolated proteinuria

A

Glomerular
Tubular
Overflow
Post renal

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14
Q

What is isolated proteinuria

A

Persistent proteinuria in absence of other urinary abnormality and normal renal functioon
Non nephrotic in range <3.5 g/day

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15
Q

Benigin causes of proteinuria

A

Transietn - young patients - absent on repeat testing and exercise precipitates
Orthostatic proteinuria - presence only in upright position

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16
Q

Renal screen

A

Complement
ANA
ANCA
GBM
Anti-dsDNA
Myeloma screen - serum free light chains, protein electrophoresis
Anti-PLA2R AA
Virology - Hep B, C + HIV
Cryoglobulins
CK

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17
Q

What is anti-PLA2R autoantibody raised in

A

Membranous nephropathy

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18
Q

What is complement typically low in

A

Vasculitis

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19
Q

Myeloma screen

A

serum free lights chains, protein
electrophoresis

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20
Q

What is anti-dsDNA riased in

A

SLE

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21
Q

CT KUB use in glomerulonephritis

A

Rule out obstructive pathology
Assess structure of kidneys

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22
Managmenet principles for all glomerular conditions
Regular monitoring Treat underlying cuase Determine natural history eg supportive or involved treat needed Treat complications Consider RRT
23
What disease can be both nephritic and nephrotic
Membranous proliferative GN
23
What mostly causes nephrotic syndrome in young children?
Minimal change disease (90% cases under 10)
24
Causes of minimal change disease
majority are idiopathic drugs - NSAIDs Malignancy - lymphoproliferative disorders Infections eg syphilis
25
What is seen on electromicroscopy in minimal change disease
Fusion of podocyte foot processes
26
What is pulmonary renal syndrome
Diffuse alveolar haemorrhage + glomerulonephritis caused by an AI disorder - serologic tests and lung/renal biopsy
27
Treatment of pulmonary renal syndorme
Immunosupress - corticosteroids, cytotoxic drugs
28
Groups of causes of glomerular disease
Nephrotic Nephritis Chronic renal failure Rapidly progressive GN Asymptomatic haematuria/proteinura
29
What causes asymtpomatiic haemturia/proteinura
alport syndreom - hereditary nephritis
30
What is RPGN
Immune complex mediated crescenteric GN
31
Causes of RPGN
Pauci immune - ANCA + Anti- GBM (goodpasteurs) Antibody mediated crescenteric GN
32
What systemic diseases can cause nephritic syndrome
Diabetic nephropathy Amyloidosis #SLE
33
Causes of nephrotic syndrome
Systemic FSGS Membranous glomerulopathy Minimal change disease MPGN
34
Causes of nephritic syndrome
Acute post infectious GN IgA nephropathy - Bergers
35
CTDs causing glomerulonephritis
Dermatomysositis Polymyositis Progressive systemic sclerosis RA SLE
36
Systemic vasculitis causing GN
Cryoglobuniamia GPA (weheners0 Microscopic polyangitis Eosinophilic granulomatosis w polyangitis IgA ass vasculitis
37
What drug can cause GN
Propylthuouracil (for hyperthyroidis)
38
Crescenteric GN on histology
Darker purple area on R side of lomerulus
39
Cardinal feature of GN
Haematuria + red cell casts in urine
40
Aetiological factors for GN
bacteria: Staphylococcus spp. Lancefiled group A B-haemolytic streptococci Streptococcus viridans Treponema pallidum viruses: Coxsackie virus Epstein Barr virus hepatitis B virus measles mumps parasites: Plasmodium malariae Schistosoma spp. drugs: penicillamine host antigens: cryoglobulin DNA tumour antigens
41
What disease does complement mediated glomerular damage occur in
Proliferative GNs
42
How long after infection does post strep GN occur
7-14 dyas after group A beta haemolytic strep - usually strep pyogene. Often URTI
43
What causes post strep GN
Immune complex - IgG, IgM, C3 dpeosition in glomeruli. Most common in young childrne
44
Features of post strep GN
general headache malaise visible haematuria proteinuria this may result in oedema hypertension oliguria
45
Bloods in post strep GN
Raised anti streptolysin O titre - confirm recent strep infetion Low C 3
46
Features of post strepGN on biopsy
acute, diffuse proliferative glomerulonephritis endothelial proliferation with neutrophils electron microscopy: subepithelial 'humps' caused by lumpy immune complex deposits immunofluorescence: granular or 'starry sky' appearance
47
What are anti-GBM antibodies
Atibodies against Type IV cl=ollagen
48
What gene is anti-GBM ass with
HLA-DR2
49
What is goodpasteurs and who common in
Rare small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis Men 2;1, bimodal age- 20-30 and 60-70.
50
Features of goodpasteurs syndrome
pulmonary haemorrhage rapidly progressive glomerulonephritis this typically results in a rapid onset acute kidney injury nephritis → proteinuria + haematuria
51
Investigations for glomeruloneprhtitis
Renal biopsy - linear IgG deposite basement membrane Raised transfer factor - pulm haemorrahge
52
Management of goodpasteurs
Plasma exchagne #Steroids Cyclophosphamide
53
How does membranous GN present
Nephrotic syndrome + proeinuria
54
Rena biopsy in membranous GN
electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. 'spike and dome' appearance
55
Causes of mebranous GN
Idiopathic 0 anti-phospholipase A2 antibodies Infection - hep B, malaria, syphilis Malignancy - prosteate, kung, lymohoma, leukaemia Drugs - gold, penicillamine, NSAIds AI - SLE (class V) , thryoiditis, rheumatoid
56
Managemnet of membranous GN
ACEi or ARB - reduce proteinuria Immunosupression = only if severe or progressive Corticosteroids + cyclophosphamide Anticoag if high risk
57
Prognsosis of membranous GN
1/3 - spontaneous remission 1/3 - reamin proeinuric 1/3 - end stage renal failure Female, young and asymptomatic modest proteinuria are good prongoses
58
Causes of focal segmental glomuerulosclerosis
Idiopathic Renal pathology eg IgA or reflux nephropathy HIV heroin Alports syndrome Sickle cell High recurrence in renal transplants
59
Renal biopsy of FSGS
focal and segmental sclerosis and hyalinosis on light microscopy effacement of foot processes on electron microscopy
60
Treatmet and prognosis FSGS
Steroids + immunosupressants if needed Untreated <10% chance remission
61

GI, liver, kidney (50 decks)

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