psc2019 > lecture 11 (renal) > Flashcards

lecture 11 (renal) Flashcards

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1
Q

what is filtered in glomerular filtration?

A
  • all plasma constituents except large proteins
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2
Q

what does the filtration barrier restrict?

A
  • solute movement based on MW, effective ratio and charge
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3
Q

what percent of cardiac output do the kidneys receive?

A
  • 25%
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4
Q

what is the glomerular filtration rate ?

A
  • 180 litres/day
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5
Q

what should be filtered?

A
  • water
  • Na+, K+, Ca2+, Cl-
  • glucose
  • urea
  • NH4+
  • creatinine
  • uric acid
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6
Q

what shouldn’t be filtered?

A
  • red blood cells
  • serum albumin
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7
Q

what is the filtration barrier made up of?

A
  • capillary endothelium
  • basement membrane
  • epithelium of bowmans capsule
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8
Q

what is the criteria for chronic kidney disease?

A
  • kidney damage for more than 3 months
  • structural or functional abnormalities of kidney
  • with or without decreased GFR
  • manifest by either pathologic abnormalities or markers of kidney damage
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9
Q

what is the easiest way to detect kidney damage?

A
  • dipstick urinalysis
  • only works if kidneys very damaged/progressed kidney disease
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10
Q

what does an eGFr of 90+ mean?

A
  • stage 1 chronic kidney disease
  • normal kidney function
  • urine findings or structural abnormalities or genetics point to kidney disease
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11
Q

what does an eGFr of 60-89 mean?

A
  • stage 2
  • mildly reduced kidney function
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12
Q

what does an eGFr of 30-59 mean?

A
  • stage 3a = 45-59
  • stage 3b = 30-44
  • moderately reduced kidney function
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13
Q

what does an eGFR of 15-29 mean?

A
  • stage 4
  • severely reduced kidney function
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14
Q

what does an eGFR of below 15 or dialysis mean?

A
  • stage 5
  • very severe
  • usually end stage kidney failure
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15
Q

what are some different autoimmune kidney diseases?

A
  • membranoproliferazive glomerulonephritis (MPGN)
  • atypical haemolytic uraemia syndrome (aHUS)
  • lupus nephritis (SLE)
  • IgA nephropathy (IgAN)
  • goodpastures syndrome
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16
Q

what is membranoproliferazive glomerulonephritis (MPGN)?

A
  • proliferation of cells in mesangium
  • thickening of glomerular basement membrane
  • reduced space
  • body defence system doesnt work properly
  • kidneys begin to fail
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17
Q

what is membranoproliferazive glomerulonephritis (MPGN) type 2?

A
  • dense deposit disease within the membrane
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18
Q
A
  • classical pathway activated by antibodies
  • ## MBL pathway deals with apoptotic and damaged cells
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19
Q

what occurs when MAC complex is recognised?

A
  • nucleated cell can internalise/get rid of the MAC
  • barrier
  • can activate cell and drive proliferation of the cell
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20
Q

what are anaphylatoxins?

A
  • small fragments of C3a and C5a
  • important in activating complement system
  • interact with molecules leading to vasodilation
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21
Q

where is c3 and c4 made?

A
  • liver mostly
  • kidney produces 20%
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21
Q

what does c3 do?

A
  • destroys microbes/pathogens
  • abundant
  • potential to cause damage
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22
Q

what is the purpose of factor H?

A
  • dampens down the effects
  • works with factor I to inactive c3 and control it
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22
Q

what occurs in chronic kidney disease to levels of complement?

Study These Flashcards
A
  • release of chemokine sand cytokines
  • allow increased production of complement
23
what are the natural C regulators?
- CR1 - MCP and DAF - CD59 prevents MAC - C1inh stops C4 binding protein
24
what does complement receptor 1 allow?
- allows immune molecules to bind to compliment to be carried to liver - for compliment disposal
25
how else can the body dispose of complement system?
- through apoptotic cells - maintain DNA and antigens within cell when they apoptosis - seen as bacterial by own immune system
26
what is complement critical for?
- normal health - self tissue renewal - bone regeneration
27
what does complement play a key role in?
- trafficking of hematopoietic stem/progenitor cells
28
what is C3a used for?
- shuts down level fo blood neutrophils - destructive
29
what is c3 glomerulopathy (C3G)?
- spectrum of disorders with glomerular pathology associated with C3 deposition - associated with defective complement action and regulation - glomeruli accumulation or deposition of c3 cleavage fragments but no immunoglobulin deposition
30
what does factor H deficiency do?
- factor H binds to glomerular basement membrane - primary defence. molecule against complement system - loss of factor H drives dense deposit disease (C3G)
31
what happens if factor H is removed?
- break off amplification loop and goes out of control - all complement is consumed
32
what is acquired C3 defieicnies?
- autoantibodies that dysregulate complement alternative pathway - make activation loop work out of control - stabilse c3 convertase and stop it being broken down - stops runaway c3b production
33
what does c3 deficiency cause?
- C3G
34
what do Factor H autoantibodies do?
- interacts with regulator - stops over activation of alternative pathway
35
what occurs in complement mediated MPGN?
- injury proliferation - reparative phase
36
what is haemolytic uraemia syndrome recognised as?
- acute renal failure - thrombocytopenia - microangiopathic haemolytic anemia
37
who does haemolytic uraemia syndrome usually affect?
- infants and young children
38
what is HUS caused by?
- shiga toxin producing E.coli
39
what occurs with the shiga toxin?
- molecules get into gut causing dmamage - problem when reaches kidney by entering bloodstream - binds to GABA3 receptor in glomerular endothelial surface activating the cells - turns to inflamed endothelial cell so allows thrombus
40
what is atypical HUS caused by?
- complement mediated TMA
41
what is secondary HUS associate with?
- stem cell transplant - pregnancy - drug associated - malignant hypertension - sepsis - autoimmune disorders - malignancy
42
what is the process involved in thrombosis?
- blood clots block veins or arteries - platelet plugging - activation of coagulation cascade - formation of fibrin plug and final clot
43
what are the environmental triggers for aHUS?
- cancer - pregnancy - drugs - pancreatitis - parasites - vaccination - autoimmune disease - cobalamin deficiency
44
what are the inherited complement abnormalities in aHUS?
- complement gene mutation of CFH - present in heterozygosity
45
what is spontaneous haemolytic ureic syndrome triggered by?
- complement factor H lacking surface recognition domains
46
what is evidence of haemolytic and thrombocytopenia?
- decreased levels of platelets - reduced sites in blood
47
what are the histological changes in TMA?
- kidney destroyed through fibrin - scaring and loss of renal function - extreme damage with collagen and fibrin deposition
48
what is essential in aHUS?
- MAC
49
what is systemic lupus erythematosus (SLE)?
- chronic inflammatory systemic autoimmune disease - unknown etiology
50
what is SLE characterised by?
- polyclonal B cell activation - abnormal autoantibodies
51
what is the pathophysiology of SLE?
- no c1q = likely to have SLE - deposition of antibodies in immune complexes, site for activation of compliment system - causes release of immune molecules (inflammatory and c3a,c5a) - drives proliferation of cells - influx of immune cells leading to destruction of glomerulus
52
which pathway is amplified in SLE?
- alternative
53
what does IgA nephropathy cause?
activation of local and systemic renin angiotensin system and complement activation - ultimately contributes to glomerulosclerosis and tubulo-interstitial fibrosis
53
what is IgA nephropathy?
- immune complex disease - IgA protein build up and damaging of filtration and glomerulus - most common - galactose deficient is genetic disorder
54
what is goodpastures syndrome?
- disease of kidney - autoantibody response to collagen chain - autoantibody develops through mimicry so attacks own cells - activates classical pathway on glomerular basement membrane
55
what does a failed reparative phase lead to?
- fibrosis - end stage renal failure (ultimately)
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