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Flashcards in 1. Glomerulonephritis Deck (34)
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1
Q

nephrotic syndrome is characterised by

A

proteinuria - typically >3g/24hr
hypoalbuminaemia - typically serum album <25g/L
oedema
hyperlipidaemia

2
Q

what happens in the kidney in nephrotic syndrome

A

glomerular basement membrane damage and increased pore size leads to increased permeability of glomerular filter to albumin
capillary walls become permeable to proteins of higher molecular weights, as severity of injury continues
loss of albumin

3
Q

what happens in hypoalbuminaemia

A

heavy proteinuria leads to low plasma albumin
colloid osmotic pressure is not maintained. so less fluid moves back into capillaries
stimulates RAAS- leads to further water and Na+ retention

4
Q

complications from nephrotic syndrome

A

immunosuppression - immunoglobulins lost in urine
hypercoagulable - controlling proteins lost in urine – increases risk of DVT, PE, renal vein thrombosis
hyperlipidaemia - increases risk of vascular disease, IHD

5
Q

management options in nephrotic syndrome

A
BP control 
ACE inhibitors to reduce proteinuria 
control hyperlipdaemia 
if hypercoagulable - anticoagulation 
treat underlying condition if possible
6
Q

primary causes of nephrotic syndrome

A

minimal change disease
membranous glomerulonephropathy
membranoproliferative GN
focal segmental glomerulosclerosis

7
Q

secondary causes of nephrotic syndrome

A
HSP (Henoch-Schlönlein purpura)
SLE 
tumour amyloid 
diabetes mellitus drugs, e.g. penicillamine
bacterial endocarditis 
congenital nephrotic syndrome
8
Q

minimal change disease causes/associations

A
cause unknown 
associated with:
- NSAIDs
- lithium/gold 
- post allergy 
- Hodgkin's
9
Q

minimal change disease histology

A

no significant change under light microscopy

under electron microscopy: podocyte fusion (foot process effacement)

10
Q

minimal change disease presentation

A

frothy urine
low albumin
preserved renal function
= nephrotic syndrome

11
Q

minimal change disease treatment

A
corticosteroids 
calcineurin inhibitors (tacrolimus)
12
Q

membranous glomerulonephropathy histology

A

sub-epithelial deposition of immune complexes
basement membrane thickening, widespread (caused by immunoglobulin deposition)
abnormal mesangial matrix causes hyalinisation of glomerulus and death of individual nephrons

13
Q

membranous glomerulonephropathy causes

A
  • idiopathic (85%)
  • autoimmune disease: SLE, RA, ankylosing spondylitis, post transplant
  • infection: hep B, syphilis, hep C, malaria
  • drugs: mercury, captopril, gold, heroin
14
Q

membranous glomerulonephropathy presentation

A

nephrotic syndrome

AKI / CKD

15
Q

membranous glomerulonephropathy treatment

A

underlying cause
steroids
calcineurin inhibitors

16
Q

focal segmental glomerulosclerosis presentation

A

proteinuria or nephrotic syndrome
later develop: haematuria and hypertension
most develop CKD within 10 years

17
Q

focal segmental glomerulosclerosis causes

A

primary
- idiopathic
secondary
- familial - reoccurs after transplantation
- virus - HIV
- drugs - heroin, pamidronate
- obesity, HTN, atheroemboli, sickle cell anaemia

18
Q

focal segmental glomerulosclerosis treatment

A

primary and familial: immunosuppression and BP control

treat secondary underlying cause

19
Q

symptoms and signs of nephritic syndrome

A
oliguria/anuria
hypertension 
fludi retention - seen as facial oedema 
haematuria - microscopic or macroscopic
uraemia 
proteinuria 

patients may also complain of: loin pain, headache, general malaise

20
Q

nephrotic vs nephritic syndrome

A

nephrotic: characterised by massive loss of protein causing various complications
nephritic: may be some proteinuria, more importantly there is haematuria, oliguria and hypertension

21
Q

primary causes of nephritic syndrome

A

mesangial proliferative GN
diffuse proliferative GN
crescentic (rapidly progressive) GN
membranoproliferative / mesangial capillary GN

22
Q

secondary causes fo nephritic syndrome

A

SLE
Wegner’s granulomatosis
microscopic polyangiitis

23
Q

mesangial proliferative GN causes

A

can occur in several diseases: IgA nephropathy, IgM nephropathy, lupus

24
Q

mesangial proliferative GN presentation

A

variable
haematuria
nephrotic syndrome?
AKI / CKD

25
Q

mesangial proliferative GN treatment

A

depends on cause
steroids
mycophenolate mofetil
cyclophosphamide

26
Q

diffuse proliferative GN

A

IgG, IgM, C3 deposition

presents with AKI, haematuria

27
Q

diffuse proliferative GN causes + treatment

A

endocarditis
post-streptococcal GN
treat underlying infection

28
Q

crescentic GN (rapidly progressive) histology

A

fibirin leaks, stimulating endothelial cells and macrophages in Bowman’s capsule to proliferate and create crescent shaped masses
reduces glomerular blood glow
seen as a part os systemic illness

29
Q

crescentic GN causes

A

ANCA-associated - related to small vessel vasculitis
- granulomatosis with polyangiitis, Wegner/s granulomatosis
- GDM disease (Goodpasteurs)
aggressive IgA nephropathy

30
Q

crescentic GN treatment

A
strict BP control 
ACE inhibitors for proteinuria >1g/day 
immunosuppression:
- steroids
- cyclophosphamide 
- mycophenolate mofetil 
- rituximab
31
Q

membranoproliferative / mesangial capillary GN histology

A

diffuse global membrane thickening and mesangial proliferation

32
Q

membranoproliferative GN presentation

A

asymptomatic haematuria or combined with nephrotic/nephritic syndrome

33
Q

membranoproliferative GN causes

A

primary (mostly)

secondary: hep C, endocarditis, viral infections, malaria, sickle cell disease

34
Q

membranoproliferative GN treatment

A
strict BP control 
ACE inhibitors for proteinuria >1g/day 
immunosuppression:
- steroids 
- calcineurin inhibitors 
- mycophenolate mofetil 
- rituximab