AKI Flashcards
what is the definition of AKI
an abrupt (<48 hrs) reduction in kidney function;
- an absolute increase in serum creatinine by >26.4 micromol/l
- or increase in creatinine by >50%
- or a reduction in urine output
can only be applied following adequate fluid resuscitation and exclusion of obstruction
what are the stages of AKI
1- (increase in serum creatinine >26 micrommol/l or increase > 1.5-1.9 x reference Cr. OR urine output <0.5 mL/hg/hr for >6 hrs)
2- increase >2-2.9 x reference SCr OR uo < 0.5 ml/kg/hr for >12 hrs
3- increase >3 x reference SCr or increase to >/= 354 micromol/L OR need for RRT. OR UO < 0.3 m/kg/hr for >24 hrs OR 12 hours anuria
what are the risk factors for AKI
patient: old age CKD diabetes cardiac failure liver disease PVD previous AKI
exposure: hypotension hypovoleamia sepsis deteriorating NEWS recent contrast medications (e.g. gentamicin)
what are the types of causes of AKI
pre renal (functional) renal (structural) post renal (obstruction)
what are the pre renal causes of AKI
hypovolaemia (haemorrhage, volume depletion (D&V, burns)
hypotension (cardiogenic shock, distributive shock (sepsis, anaphylaxis)
renal hypoperfusion (NSAIDs/ COX-2, ACEi/ARBs, heptorenal syndrome)
what is a pre renal AKI
a reversible volume depletion leading to oliguria and increase in creatinine
what is normal urine output and oliguria
normal= 0.5/kg/hr oliguria= <0.5 mls/kg/hr
what test is most sensitive for pre renal aki
urine output
what is the normal reaction to decreased renal perfusion
release of renin- increases angiotensin II- vasoconstricts efferent arteriole to maintain glomerular flow and GFR
how do ACEi affect GFR
prevent vasoconstriction of efferent arteriole in response to reduced renal perfusion- reduced GFR
how can an ACEi cause acute renal failure
as if decreased renal perfusion ACEi will exacerbate this causing a major fall in GFR
how much of cardiac output do the kidneys receive
20%
what does untreated pre renal AKI lead to
acute tubular necrosis
what is the commonest form of AKI in hospital
acute tubular necrosis
what causes acute tubular necrosis
factors leading to decreased renal perfusion
- sepsis
- severe dehydration
- rhabdomyolysis
- drug toxicity
what is the treatment for pre renal AKI
assess for hydration (BP, HR, UO, JVP, cap refil, oedema)
fluid challenge for hypovolaemia
-crystalloid (0.9% NaCl) or colloid (gelofusin)
DO NOT GIVE DEXTROSE
give bolus then reassess
if >1litre and no improvement seek help (inotropes, vasopressors)
why dont you give dextrose (hartmans) in pre renal AKI
as has potassium in it and common to get hyperkalaemic in pre renal AKI
what is renal AKI
diseases causing inflammation or damage to cells causing AKI
(blood vessels, glomerular disease, interstitial injury, tubular injury)
what are the vascular causes of renal AKI
vasculitis, renovascular disease (same as IHD but in kidneys)
what are the glomerular causes of renal AKI
glomerulonephritis
what can cause interstitial nephritis causing renal AKI
drugs- penicillin, NSAIDs, PPIs
infection (TB)
sarcoidosis
what can cause tubular injury causing renal AKI
ischaemia (prolonged renal hypoperfusion)
drugs (e.g. gentamicin)
contrast
rhabdomoyolysis