Acute kidney injury Flashcards
How is AKI defined?
increase in S creatinine by >26.5 micromole in 48 hrs
increase in S creatinine by 1.5x in 7 days
urine volume <0.5ml/kg/hr for 6 hours
Immediately dangerous consequences of AKI (AEIOU)
acidosis electrolyte imbalance intoxication overload uraemic complications
Short term consequences of AKI
hospital stay, dialysis, death,
Long term consequences of AKI
CKD, death, dialysis, CKD related CVS events
Pre-renal causes of AKI
Hypovolaemia - diarrhoea and vomit, haemorrhage, dehydration
sepsis
hypotension
congestive cardiac failure/liver failure
arterial occlusion
vasomotor eg NSAIDS, ACEI
Renal causes of AKI
acute tubular necrosis - ischaemia
toxin related eg NSAIDS, aminoglycosides, contrast
acute glomerulonephritis
acute interstitial nephritis eg PPI’s
myeloma
intra-renal vascular obstruction eg vasculitis
Post renal causes of AKI
intraluminal eg clot, calculus
intramural eg malignancy, stricture, fibrosis, Prostate disease
extramural eg malignancy, RPF
Why does pre-renal causes lead to acute tubular necrosis?
poor perfusion and lack of circulation to provide sufficient plasma flow to maintain blood chemistry and fluid balance
Is the medulla hypoxic?why?
yes
receives 10-15% of renal blood flow
metabolically active
initiation of tubular necrosis
exposure to toxic/ischaemic insult
pre-renal parenchymal injury evolving but AKI preventable
Maintenance of tubular necrosis
established parenchymal injury and max. oliguric
1-2 weeks –> several months
Recovery of tubular necrosis
gradual increase in urine output and fall in serum creatinine
What happens if GFR recovers quicker than tubule resorptive capacity?
excessive diuresis
What is radiocontrast nephropathy?
hospital AKI following iodinated contrast agent
Risk factors for radiocontrast nephropathy
DM renovascular disease paraprotein impaired renal function high volume of radiocontrast