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GI, liver, kidney > Glomerulonephritis > Flashcards

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
Q

Managmenet principles for all glomerular conditions

A

Regular monitoring
Treat underlying cuase
Determine natural history eg supportive or involved treat needed
Treat complications
Consider RRT

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23
Q

What disease can be both nephritic and nephrotic

A

Membranous proliferative GN

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23
Q

What mostly causes nephrotic syndrome in young children?

A

Minimal change disease (90% cases under 10)

24
Q

Causes of minimal change disease

A

majority are idiopathic
drugs - NSAIDs
Malignancy - lymphoproliferative disorders
Infections eg syphilis

25
Q

What is seen on electromicroscopy in minimal change disease

A

Fusion of podocyte foot processes

26
Q

What is pulmonary renal syndrome

A

Diffuse alveolar haemorrhage + glomerulonephritis caused by an AI disorder - serologic tests and lung/renal biopsy

27
Q

Treatment of pulmonary renal syndorme

A

Immunosupress - corticosteroids, cytotoxic drugs

28
Q

Groups of causes of glomerular disease

A

Nephrotic
Nephritis
Chronic renal failure
Rapidly progressive GN
Asymptomatic haematuria/proteinura

29
Q

What causes asymtpomatiic haemturia/proteinura

A

alport syndreom - hereditary nephritis

30
Q

What is RPGN

A

Immune complex mediated crescenteric GN

31
Q

Causes of RPGN

A

Pauci immune - ANCA +
Anti- GBM (goodpasteurs)
Antibody mediated crescenteric GN

32
Q

What systemic diseases can cause nephritic syndrome

A

Diabetic nephropathy
Amyloidosis
#SLE

33
Q

Causes of nephrotic syndrome

A

Systemic
FSGS
Membranous glomerulopathy
Minimal change disease
MPGN

34
Q

Causes of nephritic syndrome

A

Acute post infectious GN
IgA nephropathy - Bergers

35
Q

CTDs causing glomerulonephritis

A

Dermatomysositis
Polymyositis
Progressive systemic sclerosis
RA
SLE

36
Q

Systemic vasculitis causing GN

A

Cryoglobuniamia
GPA (weheners0
Microscopic polyangitis
Eosinophilic granulomatosis w polyangitis
IgA ass vasculitis

37
Q

What drug can cause GN

A

Propylthuouracil (for hyperthyroidis)

38
Q

Crescenteric GN on histology

A

Darker purple area on R side of lomerulus

39
Q

Cardinal feature of GN

A

Haematuria + red cell casts in urine

40
Q

Aetiological factors for GN

A

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
Q

What disease does complement mediated glomerular damage occur in

A

Proliferative GNs

42
Q

How long after infection does post strep GN occur

A

7-14 dyas after group A beta haemolytic strep - usually strep pyogene. Often URTI

43
Q

What causes post strep GN

A

Immune complex - IgG, IgM, C3 dpeosition in glomeruli. Most common in young childrne

44
Q

Features of post strep GN

A

general
headache
malaise
visible haematuria
proteinuria
this may result in oedema
hypertension
oliguria

45
Q

Bloods in post strep GN

A

Raised anti streptolysin O titre - confirm recent strep infetion
Low C 3

46
Q

Features of post strepGN on biopsy

A

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
Q

What are anti-GBM antibodies

A

Atibodies against Type IV cl=ollagen

48
Q

What gene is anti-GBM ass with

A

HLA-DR2

49
Q

What is goodpasteurs and who common in

A

Rare small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis
Men 2;1, bimodal age- 20-30 and 60-70.

50
Q

Features of goodpasteurs syndrome

A

pulmonary haemorrhage
rapidly progressive glomerulonephritis
this typically results in a rapid onset acute kidney injury
nephritis → proteinuria + haematuria

51
Q

Investigations for glomeruloneprhtitis

A

Renal biopsy - linear IgG deposite basement membrane
Raised transfer factor - pulm haemorrahge

52
Q

Management of goodpasteurs

A

Plasma exchagne #Steroids
Cyclophosphamide

53
Q

How does membranous GN present

A

Nephrotic syndrome + proeinuria

54
Q

Rena biopsy in membranous GN

A

electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. ‘spike and dome’ appearance

55
Q

Causes of mebranous GN

A

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
Q

Managemnet of membranous GN

A

ACEi or ARB - reduce proteinuria
Immunosupression = only if severe or progressive
Corticosteroids + cyclophosphamide
Anticoag if high risk

57
Q

Prognsosis of membranous GN

A

1/3 - spontaneous remission
1/3 - reamin proeinuric
1/3 - end stage renal failure
Female, young and asymptomatic modest proteinuria are good prongoses

58
Q

Causes of focal segmental glomuerulosclerosis

A

Idiopathic
Renal pathology eg IgA or reflux nephropathy
HIV
heroin
Alports syndrome
Sickle cell
High recurrence in renal transplants

59
Q

Renal biopsy of FSGS

A

focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy

60
Q

Treatmet and prognosis FSGS

A

Steroids + immunosupressants if needed
Untreated <10% chance remission

61
Q
A

GI, liver, kidney (50 decks)

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