acute kidney dysfunction Flashcards
AKI
abrupt loss of kidney function
leads to retention of urea and other nitrogenous waste and dysregulation of ECV and electrolytes
even very small increases in serum creatinine are ass. w/ worse outcomes
aetiology
due to pre-renal in 90%
typically hypotension ss. w/ sepsis and/or fluid depletion
can be further exacerbated by ACE-i, or NSAIDs, which affect the kidney’s response to hypotension
prerenal
volume depletion - haemorrhage, severe vomiting, diarrhoea, burns, inappropriate diuresis
oedematous states - cardiac failure, cirrhosis, nephrotic syndrome
hypotension - cardiogenic shock, sepsis, anaphylaxis
CV - severe cardiac failure, arrhythmias
renal hypoperfusion - NSAIDs, COX-2 inhibitors, ACE-i, angiotensin-II receptor agonists (ARBs), AAA, renal artery stenosis or occlusion, hepatorenal syndrome
renal
glomerular disease - glomerulonephritis, thrombosis, haemolytic uraemic syndrome
tubular injury - acute tubular necrosis (ATN) following prolonged ischaemia, nephrotoxins (eg aminoglycosides, radiocontrast media etc)
acute interstitial nephritis due to drugs (NSAIDs), infection or autoimmune
vascular disease - vasculitis, cryoglobnulinaemia, polyarteritis nodosa, thrombotic microangiopathy
eclampsia
postrenal
calculus blood clot papillary necrosis urethra stricture prostatic hypertrophy/malignancy bladder tumour radiation fibrosis pelvic malignancy retroperitoneal fibrosis
epidemiology
15% of adults admitted to hospital develop AKI
particularly common in the elderly
risk factors in people with acute illness
age >65yo
CKD, particularly if eGFR <60
past Hx AKI
co-existing illness, eg cardiac failure, liver disease, diabetes
neuro impairment or disability (reduced access to fluids - same in young children)
hypovolemia
Sx/Hx/risk factors for urological obstruction
sepsis
use of iodinated contrast media in the previous week
NSAIDs, ACE-i, ARBs
deteriorating NEWS
peri-operative patients
presentation
depends on underlying cause and severity
clinically: decreased urine output, rise in serum creatinine
AKI associated with at least one of the following:
rise in serum creatinine of 26umol/L or greater within 48h
50% or greater increase in serum creatinine (1.5 fold from baseline) within the preceding 7 days
fall in urine output to less than 0.5ml/kg/hr for more than 6h
Sx
urine output:
oliguria, anuria
may also cause polyuria due to fluid reabsorption by damaged renal tubules, or osmotic effect of accumulated metabolites
abrupt anuria suggests obstruction, acute and severe glomerulonephritis, or acute renal artery occlusion
gradual diminution of urine output may indicate a urethral stricture or bladder outlet obstruction
n&v
dehydration
confusion
signs
HTN
abdo: may reveal a large, painless bladder typical of chronic urinary retention
dehydration with postural hypotension and no oedema
fluid overload with raised JVP, pulmonary oedema or peripheral oedema
pallor, rash, bruising
pericardial rub
DDx
acute on chronic CKD suggested by: long duration of Sx nocturia absence of acute illness anaemia hyperphosphatemia, hypocalcaemia reduced renal size reduced cortical thickness
management
largely supportive treat cause where possible monitor fluids and electrolytes fluid therapy stop nephrotoxic drugs urgent relief of urinary tract obstruction
complications
if unrecognised, AKI will lead to: progressive uraemia (toxic waste accumulation) metabolic acidosis hyperkalaemia spontaneous haemorrhage pulmonary oedema
prognosis
indicators of poor prognosis: older age multiple organ failure oliguria hypotension acute on chronic number of transfusions
dialysis linked to higher mortality (reflection of the condition, not the treatment)
increased stage of AKI
