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weenal > glomelOnef > Flashcards

glomelOnef Flashcards

1
Q

what is gn

A

immune-mediated disease of the kidneys affecting the glomeruli (w/ secondary tubulointerstitial damage)

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2
Q

pathogenesis of gn

A

humoral (antibody-mediated)
- intrinsic or planted antigen
- deposition of circulating immune complexes

cell-mediated (t-cells)

inflammatory cells, mediators and complements

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3
Q

significance of glom cap wall

A

size and charge selective barrier
(in gn - disruption of barrier leads to haematuria and/or proteinuria)

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4
Q

damage to endothelial or mesangial cells leads to…

A

a proliferative lesion and red cells in urine

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5
Q

damage to podocytes leads to…

A

a non-proliferative lesion and protein in urine

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6
Q

**cells of nephron respond to injury in different ways

A
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7
Q

diagnosing gn through ____

A

clinical presentation
blood tests
examination of urine
kidney biopsy

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8
Q

specific exams of urine for rn

A

urinalysis - haematuria
urine microscopy - rbc (dysmorphic), rbc & granular casts, lipiduria
urine protein - creatinine ratio/24hr urine - quantify proteinuria

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9
Q

clinical renal presentations

A

haematuria (red cells in urine)
- asymptomatic microscopic haematuria
- episodes of painless macroscopic haematuria

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10
Q

proteinuria/albuminuria

A

microalbuminuria (30-300mg albuminuria/day)
asymptomatic proteinuria (<1 g/day)
heavy proteinuria (1-3 g/day)
nephrotic syndrome (> 3 g/day))

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11
Q

what do rbcs look like in gn

A

dysmoprphic (squishy squashy squashed squashers)

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12
Q

NEPHR(iiiiiiiii)tic syndrome

A

acute decline in kidney function
oliguria
oedema caused by fluid retention
hypertension
“active” urinary sediment (RBCs, RBC casts)

indicative of a proliferative process
affecting endothelial cells

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13
Q

NEPHR(ooooooo)tic syndrome

A

proteinuria > 3 g/day (mostly albumin, also globulins)
hypoalbuminaemia (<30)
oedema
hypercholesterolaemia
usually normal renal function

indicative of a non proliferative process
affecting Podocytes

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14
Q

nephr(OOOO)tic syndrome

A

infections - loss of opsonising antibodies
renal vein thrombosis
pulmonary emboli
volume depletion (overaggressive use of diuretics) - may lead to AKI (pre-renal)

vit D deficiency
subclinical hypothyroidism

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15
Q

classifications

A
  1. AETIOLOGY
    - (majority)
    - caused by eg. infections or drugs associated with eg. malignancies or part of systemic disease eg. ANCA - associated systemic vasculitis, lupus, Goodpastures, HSP
  2. HISTOLOGY
    renal biopsy
    (light microscopy/immunofluorescence/EM)
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16
Q

histological classification in GN terminology

A
  • proliferative or non-proliferative (usually refers to presence or absence of proliferation of mesangial cells)
  • focal/diffuse (< or > 50% glomeruli affected)
  • global/segmental (all or part glomerulus affected)
  • crescentic (presence of crescents - extracapillary proliferation of inflammatory cells within Bowman’s space, eg RPGN in vasculitis)
17
Q

treatment of GN principles

A

reduce degree of proteinuria
induce remission of nephrotic syndrome
preserve longterm renal function

18
Q

non immunosuppressive treatments of gn

A
  • anti-hypertensives (target BP <130/80 if proteinuria)
  • ACE inhibitors/ ARBs
  • SGLT2i
  • diuretics
  • statins
  • anticoagulants in nephrotic syndrome with profound hypoalbuminaemia
19
Q

immunsuppression treatments

A

DRUGS
- corticosteroids (Prednisolone po/MethylPred IV)
- alkylating agents (Cyclophosphamide/ Chlorambucil)
- calcineurin inhibitors (Cyclosporin/Tacrolimus)
- anti-proliferatives (azathioprine/MMF)

PLASMAPHERESIS
- (TPE-therapeutic plasma exchange)

ANTIBODIES
-IV Immunoglobulin (IVIG)
-Monoclonal Antibodies

20
Q

treatment of nephr(OOOOO)tic patients

A

GENERAL
- fluid restriction (less than 1.5l in a day)
- salt restriction
- diuretics
- ACE Inhibitors/ ARBs
- consider Anticoagulation if albumin<20
- IV Albumin (only if volume deplete) statins to try increase oncotic pressure that is in wrong place

21
Q

how many treatment nephrOOOOtic involves immunosuppression?

A

MOST

aim is to induce sustained remission
- complete remission (proteinuria < 300mg/day)
- partial remission (proteinuria <3g/day)

22
Q

idiopathic GN main types

A

minimal change
fsgs
membranous
membranoproliferative
igA nephropathy
rapidly progressive glomerulonephritis

23
Q

minimal change nephropathy

A
  • commonest cause of nephrotic syndrome in children (77%)
  • normal renal biopsy on LM & IF with foot process fusion on EM.
  • 94 % complete remission with oral steroids
  • some are steroid-resistant/ dependent or have multiple relapses
  • second-line drugs: cyclophosphamide/CSA
  • does NOT cause progressive renal failure
  • possibly caused by IL-13, anti-nephrin Ab
24
Q

fsgs

A
  • commonest cause of nephrotic syndrome in adults (35%)
  • (HIV/Heroin use/Obesity/ Reflux nephropathy) or genetic
  • renal biopsy: As its name describes on light microscopy with minimal Ig/ Complement deposition on IF
  • remission with prolonged steroids in 60 %
  • 50 % progress to end stage renal failure after 10 years
25
Q

membranous nephropathy

A
  • 2nd commonest cause of nephrotic syndrome in adults (15-30%)
  • 1 or 2
  • important 2 causes include: infections (hepatitis B/ parasites), connective tissue diseases (lupus), malignancies (carcinomas/ lymphoma), drugs (gold/penicillamine)
  • renal biopsy: subepithelial immune complex deposition in the basement membrane
  • steroids/ Alkylating agents/B cell monoclonal Ab
  • 30% progress to end stage renal failure in 10 years
26
Q

anti PLA2r antibody

A

present in >70% of primary MN

27
Q

histological appearance of membranous nephropathy

A

thickened basement membranes - silver stain

28
Q

more membranprolif glomeruloneph

A
29
Q

membranoproliferative gn

A
  • pattern of injury with different causes.
  • 2 primary mechanisms;
  • immune complex deposition and complement activation.
  • dysregulation of the alternative complement pathway.
30
Q

igA nephropathy

A
  • commonest GN in the world
  • asymptomatic microhaematuria +- non-nephrotic range proteinuria
  • macroscopic haematuria after resp/GI infection
  • AKI/ CKD
  • associated with Henoch-Schonlein Purpura (HSP) (arthritis/colitis/ purpuric skin rash)
  • renal biopsy: Mesangial cell proliferation and expansion on light microscopy with IgA deposits in mesangium on IF
  • 25% progress to end stage renal failure in 10-30 years
  • BP control/ ACE inhibitors & ARBs/ Fish oil
31
Q

immunology

A

process diagram

32
Q

iga nephropathy

A

mesangial cell proliferation and expansion (H&E stain)

33
Q

rpgn

A
  • treatable, immune mediated cause of acute kidney injury
  • rapid deterioration in function over days/weeks
  • ‘active’ urinary sediment (RBCs, RBC & Granular Casts)
  • may be part of systemic disease.
  • associated with glomerular crescents on biopsy.
34
Q

hsitologiacl buzzword

A

crescent formation

35
Q

rpgn treatment

A

treatement

weenal (18 decks)

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