AKI in Small Animal Medicine Flashcards
(80 cards)
kidneys have a high risk of
ischaemic & nephrotoxic insult
kidneys receive 25% of
cardiac output
Kidney jobs
- filter to excrete urine
- change composition of urine to excrete things they need to
kidneys are at a high risk for impaired fxn if
blood volume changes (hypovolaemia, hypotension, anaemia)
or anything that changes perfusion b/c of blood the kidneys must receive
if a toxin is ingested, it travels through
the kidney quickly
kidneys have high…
metabolic demands & nutrient requirements
Nephrotoxins can potentially accumulate in the…
tubules of the kidneys
Classic definition of AKI
serum creatinine above upper ref range
AKI is a complex…
dynamic metabolic disorder
AKI has a rapid decline in
renal fxn
AKI has retention of
uraemic waste (azotaemia)
AKI has a deranged…
fluid status (dehydration/fluid retention)
AKI has electrolyte…
imbalances & acid-base disorders
AKI is noted as what changes to creatinine?
Creatinine elevation >26.4 micromol/L OR >25% w/i 48 hrs
Grade 1 AKI (non-azotaemic AKI)
- documented AKI (hx, clinical, lab, imaging evidence, clin anuria/oliguria, vol responsiveness) &/or
- progressive non-azotaemic increase in blood creatinine w/i 48 hrs
- measured oliguria or anuria over 6 hr
Grade II AKI (mild AKI)
- documented AKI & static or progressive azotaemia
- progressive azotaemia: increase blood creatinine w/i 48 hrs or vol responsiveness
- measured oliguria or anuria over 6 hrs
(values higher than Grade I)
Grade III-V AKI (mod to severe AKI)
Documented AKI & increasing severities of azotaemia & functional renal failure
What is the continuum in AKI?
event –> decreased kidney fxn –> progression up to stage 4, some sequelae or not
Phase I of AKI
- no clin signs (non-azotaemic)
- intrinsic injury/dysfxn
- rapid haemodynamic, filtration, tubulointerstitial or outflow injury = accumulation of metabolic toxins, dysregulation of acid-base, electrolytes & ECF balance
- Duration depends on nature of primary insult
Phase 2 AKI
- cell death, cytokines, WBC –> repeats –> remodeling of tissue, cells dead replaced by fibrin; start of structural damage
- tubules 1st site for remodelling/changes -> cases in urine formed by proteins or tubular cells
- continued hypoxia & inflammation –> propagation of renal damages
- cortical structures: 90% renal blood flow + high metabolism - predisposed to damages
- intervention may not be successful
- PU/PD, increase thirst due to Na loss
Phase 3 AKI
- critical amt of damages has occurred - last few days to 1-3 wks
- remodelling continues, cannot cope, fall into full kidney failure or Phase 4
- urine output increases or decreases
- loss of tubular fxn
- oliguria, prod’n of urine abnormal, not full kidney filtration
- if you restore blood flow, remove toxins, etc. can return to recovery phase & regain fxn
Phase 4 AKI
- depends on how early & how well txt occurs (3 mos after AKI can regen tubules)
- increased urinary output
- vol depletion can lead to progression of kidney dz
- vol depletion can lead to progression of kidney dz
regeneration & repair of renal tissue can take mos & may not regain full fxn (CKD)
AKI results in abnormalities in..
CNS, immune, resp, haemostatic, GIT signs, dehydration from PU/PD in early stages
AKI impairs coag systems/aggregations to be
normal…