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renal disease classification Flashcards

(60 cards)

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1
Q

most common cause of chronic Renal failure requiring dialysis/renal transplantation

A
  • diabetes
  • glomerulonephritis
  • hypertension
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2
Q

clinical presentation of renal disease

A
  • acute renal failure
  • chronic renal failure
  • nephritic syndrome - rapidly progressive glomerulonephritis
  • nephrotic syndrome
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3
Q

acute renal failure presentation

A
  • azotaemia/uraemia
  • usually accompanied by oliguria/anuria
  • may completely resolve or progress to chronic renal syndrome
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4
Q

azotaemia

A

rise in serum urea and creatinine

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5
Q

serum creatinine is a marker of

A

renal function

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6
Q

uraemia

A

azotaemia becoming symptomatic

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7
Q

oligourea

A

drop in urine volume

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8
Q

anuria

A

failure to urinate completely

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9
Q

chronic renal failure presentation

A

gradual rise in serum urea/creatinine
symptoms and signs of renal dysfunction
eventual progressioon to end stage renal failure eGFR <5%
requiring dialysis/transplantation

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10
Q

clinical manifestations of renal dysfunction

A 
lethargy 
anorexia 
SOB 
peripheral neuropathy 
oedema
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11
Q

pre renal cause of renal failure

A

anything impairing renal perfusion

  • drop n blood volume
  • cardiac shock
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12
Q

renal causes of renal failure

A

disease intrinsic to the kidney

  • glomerulonephritis
  • acute tubular necrosis
  • scute interstitial nephritis
  • tumour lysis syndrome
  • drug induced nephrotoxicity
  • contrast-induced nephropathy
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13
Q

post renal causes of renal failure

A

anything obstructing urine outflow

  • stones
  • stricture due to radiotherapy or trauma
  • due to aa tumour growing in the retroperitoneum
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14
Q

nephritic syndrome

A
  • azotaemia/uraemia
  • oliguria
  • haematuria - often macroscopic - mild to moderate proteinuria
  • hypertension
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15
Q

nephritic syndrome usually due to

A

glomerularnephritis

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16
Q

rapidly progressive glomerulonephritis

A

RPGN

  • subset of nephritic syndrome
  • rise in serum level creatinine/urea is rapid and severe
  • usually due to crescentic glomerulonephritis
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17
Q

RPGN is a subset of

A

nephritic syndrome

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18
Q

nephrotic syndrome

A
  • proteinuria
  • hypoalbuminaemia
  • peripheral oedema
  • hyperlipidaemia
  • lipduria
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19
Q

mechanisms of nephrotic syndrome

A

increased glomerular capillary permeability - leaky
low serum protein - leaks into urine
reduced serum oncotic pressure
increased hepatic lipid synthesis - liver attempts to compensate

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20
Q

oncotic pressure

A

the ability of the vascular system to maintain fluid within the vascular system

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21
Q

pitting oedema

A

pressing down on the skin leaves an imprint

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22
Q

Dendant oedema

A

accumulates in areas under gravitational force

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23
Q

pathogenesis of glomerular nephritis

A

2 main pathogeneses

  • immune complexes
  • structural abnormalities - usually in podocytes, podcytopathy
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24
Q

immune complex pathogenesis of glomerulonephritis

A

proteins become trapped
immune complexes in thee mesangium - masangial cells proliferate causing mesangial hypercellularity and mesangial matrix expansion
immune complexes in sub endothelial space - between the endothelium and glomerular basement membrane, glomerulus proliferates endothelial cells, endothelial proliferation
immune complexes in the epimembranous/subepithelial space - glomerulus produces new basement membrane called ‘spikes’

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25
diagnostic core biopsy
- light microscopy - electron microscopy - immunoflourescence
26
immunofluorescence
manufactured antibodies with fluorescent signal attatched that are specific for components of immune complexes
27
primary glomerulonephritis
no identifiable cause | idiopathic
28
secondary glomerulonephritis
- drug - infections - autoimmune diseases - malignancy
29
minimal change disease
- type of glomerulonephritis - disease of children - structural abnormality - podocytopathy - normal glomeruli under light microscopy - no immune complexes
30
electron microscopy findings for minimal change disease
normal podocyte findings: - cytoplasmic extensions - foot processes - spaces in between called slit diaphragms - have an electrical charge which repels electrical charge in protein keeping protein in the circulation minimal change disease finings: - foot processes are fused which means slit diaphragms are lost causing protein to leak into urine causing nephritic syndrome
31
secondary causes of minimal change disease
- drugs - malignancy - vaccinations
32
prognosis of minimal change disease
- good in children - highly responsive to steroids | - poorer response in adults
33
membranous nephropathy
- usually effects adults especially Middle Ages males - immune complex mediates - nephritic syndrome/nephritic range proteinuria
34
findings for membranous nephropathy
light microscopy - circumferential thickening of glomerular capillary loops - thickening due to immune complexes - glomerulus reacts by producing new basement membrane spikes alternating with subepithelial deposits immune fluorescence - immune complexes - IgG and C3 (evidence of complement cascade) electron microscopy - subepitheial deposits - intervening basement membrane spikes
35
primary membranous nephropathy
now known to be due to autoantibodies - protein on the podocytes
36
prognosis of membranous nephropathy
generally indolent | may progress to chronic renal failure
37
focal or diffuse glomerular nephropathy
- focal affects <50% of glomeruli | - diffuse affects >50%
38
segmental and global glomerular nephropathy
segmental affects <50% of an individual glomerulus | global affects >50%
39
focal segmental glomerulosclerosis
- most common cause of nephrotic syndrome in adults structural abnormality - nephrotic syndrome.nephritic range proteinuria
40
findings of focal segmental glomerulosclerosis
focal and segmental collapse of the capillary loops with scarring and fibrous adhesions to the bowman's capsule immunofluorescence - antibodies found but not immune complex mediated, antibodies just trapped electron microscopy - segmental scarring - subtotal effacement of the podocytic foot processes
41
secondary causes of FSGS
- any cause of nephron loss - HIV, sickle cell, herion abuse, obesity - all other types of glomerulonephritis
42
prognosis of FSGS
some respond to steroids | remainder progress to chronic renal failure
43
post infectious glomerular nephritis
acute proliferative/post streptococcal glomerulonephritis - usually children - 1-4 weeks post cellulitis/pharyngitis - immune complex mediated - planted streptococcal pyogenic exotoxin (protein on the streptococcal organism)
44
findings I posy infectious glomerulonephritis
``` diffuse proliferative mesangial hypercellularity endocapillary proliferation neutropenic inflammation immunoflourescens - granular, mesangial and capillary loop IgG and C3 electron microscopy - sup epithelial 'humps' ```
45
cause of post infectious G
- always secondary - post infectious - usually S progenies - non streptococcal causes include other bacteria, viral and parasitic organisms
46
prognosis of post infectious G
most children recover with conservative treatment | adults may progress to chronic renal failure
47
IgA nephropathy
- berger's disease most common cause of G usually young adults immune complex mediated
48
clinical presentation of IgA nephropathy
microscopic haematuria/nephritic syndrome | sometimes precipitated by URTI
49
findings of IgA nephropathy
``` light microscopy diffuse mesangiaal matrix expansion and hypercellularity immunoflurescence - granular mesangial IgA electron microscopy - mesangiaal immune complex deposits ```
50
causes of IgA nephropathy
- drugs - infections - hepatobillary, GI, rheumatological diseases and malignancy
51
prognosis of IgA nephropathy
- 1/3 resolve - 1/3 stable disease - 1/3 progress to secondary FSGS/CRF
52
crescentic glomerulonephritis
pathological correlate to clinical presentation of rapidly progressive glomerulonephritis - nephritic syndrome with rapid and severe rise in serum urea/creatinine medical emergency - chronic renal failure within weeks to months untreated histological pattern - not a diagnosis
53
crescentic GN under the microscope
crescent - filing and occlusion of the bowman's space by proliferation of parietal epithelial cells - due to rupture of capillary loops - sign of severe glomerular injury
54
types of crescentic GN
- type 1 - anti glomerular basement membrane disease - type 2 - immune complex mediated - post infectious, IgAA, mesangiocapillary GN - type 3 - pauci immune GN
55
anti-GBM disease
autoantibody to a3 chain of type 4 collagen of GBM | autoantibodies may cross react with basement membrane of pulmonary alveolar ca[illaries
56
findings in anti-GBM syndrome
crescents with necrosis linear capillary loop IgG angle antibodies - no immune complexes found
57
lupus nephritis
lupus can affect the glomeruli in many ways
58
pauci-immune GN
anti neutrophil cytoplasmic antibody associated glomerulonephritis and vasculitis autoantibodies against cytoplasmic enzymes in neutrophils are released - toxic and damage endothelial cells associated with systemic small vessel vasculitis
59
two syndromes associated with pauci-immune GN
wegener's GN - necorising graanulomaatous inflammatioon of upper and lower respiratory tract and kidney charge-strauss syndrome - similar to WG with asthma and peripheral eosinophilia
60
findings in pauci-immune GN
crescents and granulomatous inflammation in Wegener's eosinophil rich granuloma in charge- Strauss syndrome no findings in immunoflourescence and no immune complexes in electron microscopy

pathology 2 (47 decks)

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