Acute Kidney Injury Flashcards
(53 cards)
what are the 6 main functions the kidneys
- body fluid homeostasis
- regulation of vascular tone
- excretory function
- electrolyte homeostasis
- acid-base balance
- endocrine function
what is the traditional definition of acute renal failure
rapid loss of glomerular filtration ad tubular function over hours to days
retention of urea/creatinine
oliguric/non-oliguric
potentially recoverable
what is the relationship between serum creatinine and GFR
as % normal GFR falls, serum creatinine levels rise
BUT
creatinine levels will only start to rise after loss of 60% of normal GFR
what is the current definition of acute kidney disease (i.e. include specific values)
an increase in serum creatinine:
- by >26.5 micro mol/l within 48hrs
OR - to >1.5 times baseline - which is known or presumed to have occurred within the prior 7 days
Urine volume <0.5 ml/kg/h for 6 hours
what are the serum creatinine levels and urine output for stage 1 acute kidney injury
SC:
1.5–1.9 times baseline
OR ≥ 26.5 μmol/l increase
URINE:
<0.5 ml/kg/h for 6–12 hours
what are the serum creatinine levels and urine output for stage 2 acute kidney injury
SC:
2.0–2.9 times baseline
URINE:
<0.5 ml/kg/h for ≥12 hours
what are the serum creatinine levels and urine output for stage 3 acute kidney injury
SC:
3.0 times baseline
OR Increase to ≥354 μmol/l (and above)
OR Initiation of renal replacement therapy
URINE:
<0.3 ml/kg/h for ≥ 24 hours OR Anuria for ≥12 hours
how many hospital admissions are complicated by AKI
1 in 5-7
more than half in ITU admissions
what are the immediate consequences of AKI
think vowels - AEIOU
A - acidosis E - electrolyte imbalance I - Intoxication TOXINS O - overload U - Uraemic complications
explain how each of the immediate dangerous consequences come about (AEIOU)
A - not reabsorbing bicarbonate - blood pH goes down = cardiac arrest
E - not reabsorbing or reabsorbing too many electrolytes - can lead to e.g. hyperkalaemia = cardiac arrest
I - toxin build up (e.g. opiates) due to not being removed from kidneys = respiratory (and then cardiac) arrest
O - fluid not being removed - fluid and pulmonary oedema = cardiac arrest
U - urea in the blood = renal failure
what are the three groups of causes for AKI
pre-renal
- blood flow to kidney
renal (intrinsic)
- damage to renal parenchyma
post-renal
- obstruction to urine exit
what are the 3 types pre-renal causes
- reduce effective circulation volume:
- sepsis
- hypovolaemia (haemorrhage, burns,
vomiting/diarrhoea, diuretics)
- hypotension (medications)
- cardiac failure - arterial occlusion
- vasomotor
- NSAIDS/ACE inhibitors
what are the 6 types of renal (intrinsic) causes
- acute tubular necrosis (ATN)
- ischaemia - toxin related
- drugs
- radiocontrast
- rhabdomyolysis (Haem pigments)
- snake venom, heavy metals, mushrooms, etc - acute interstitial nephritis
- acute glomerulonephritis
- myeloma
- intra renal vascular obstruction
- vasculitic
- thrombotic microangiopathy
what is rhabdomyolysis
when there is break down of muscle (e.g. crushing injury) and the break down products go to get filtered at the kidneys but can’t - lead to build up of toxic breakdown products
**included are harm pigments from blood so on dipstick would show blood in urine BUT under microscope would NOT show blood cells
what is the post-renal cause
obstruction
- intraluminal (calculus, clot, sloughed papilla)
- intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
- Extramural (retroperitoneal fibrosis, malignancy)
can different groups of causes occur simultaneously
yes - often several causes co-exist i.e. can have pre and intrinsic causes
what is the most common cause of AKI
poor perfusion leading to established tubule damage
what is ischaemic renal injury
tubular necrosis
what occurs in the initiation stage of ischaemic renal injury
exposure to toxic/ischaemic insult
renal parenchymal injury evolving
AKI potential preventable at this stage
what occurs at the maintenance stage of ischaemic renal injury
established parenchymal injury
usually maximally oliguric now
typical duration 1-2 weeks (but can be up to several months recovery)
what occurs at the recovery stage of ischaemic renal injury
gradual increase in urine output
fall in serum creatinine (may lag behind diuresis)
what happens if GFR recovers quicker than tubule restive capacity
excessive diuresis - eg ost obstructive natriuresis
what is radio contrast nephropathy
AKI following administration of iodinated contrast agent
usually transient renal dysfunction that resolves after 72hrs
BUT
may lead to permanent loss of function
what are risk factors for radio contrast nephropathy
Diabetes mellitus Renovascular disease Impaired renal function Paraprotein High volume of radiocontrast
