AKI Flashcards
what is an AKI
abrupt decline in renal function (GFR) occurring over hours to days, sometimes over weeks, with the inability to maintain and regulate fluid, electrolyte and acid-base balance
what labs are associated with AKI
associated with accumulation of waste products (urea and creatine)
normal urine output
> =1200ml/d
anuria urine output
<50ml/d
oliguria urine output
<500ml/d
non-oliguria urine output
> 500ml/d
KDIGO definition of AKI
- SCr increase by >=26.5 mmol/L within 48h or
- SCr increase to >=1.5x baseline within 7d or
- Urine Vol <0.5ml/kg/h for >=6h
causes of AKI
- intravascular volume depletion
- drugs (NSAIDs, ACEi, ARBs, Contrast media, ahminoglycosides, amphotericin B, antivirals, Chemo)
- infections
- cardiac
- surgery
pre renal AKI
resulting from decrease renal perfusion (most common in hospital) due to:
- volume depletion; or
- reduced cardiac output; or
- renal hypo perfusion
intrinsic AKI
result of structural damage within kidney due to:
- acute tubular necrosis (most common)
- acute interstitial nephritis
- glomerular damage
- vascular damage
post renal AKI
caused by obstruction of urine flow
risk factors for AKI
- > 60yo
- female
- acute infection
- pre existing chronic respiratory or CVD
- dehydration / vol depletion
- preexisting CKD -> AoCKD
clinical presentation of AKI
- reduced urine output
- peripheral edema
- flank pain
- abnormal labs (elevated SCr, BUN, K; presence of WBC, RBC, crystals in urine; abnormal SG, FeNA, urine osmolarity)
possible causes of volume depletion
- hemorrhage
- GI losses (vomit/diarrhea)
- Urinary losses (over diuresis, DI)
- burns, peritonitis
- decrease effective volume (cirrhosis)
- peripheral vasodilation (sepsis, vasodilator)
possible causes of reduced cardiac output
- sepsis
- CHF
- MI
- Pericardial tamponade
- Acute PE
possible causes of renal hypoperfusion
- Bilateral renal artery occlusion (thrombosis, emboli, stenosis)
- medications (ACEi, NSAIDs, calcineurin inhibitors, radiocontrast media, vasopressors)
diagnosis and evaluation for pre renal AKI
- pt hx (GI loss, diuresis)
- physical exam (orthostatic hypotension, tachycardia, poor skin turgor)
- central venous pressure (volume status of heart)
- urine test (SG, osmolarity, FeNa)
Management of AKI
- reverse etiologic factors (treat pre-renal causes)
- use vasopressors with fluids in pt w vasomotor shock
- supportive care
possible causes of acute tubular necrosis
- ischemic (hypotension, vasoconstriction)
- nephrotoxins (contrast dyes, heavy metals, amphotericin B, Aminoglycosides, organic solvents)
- endogenous toxins (hemoglobin, myoglobin)
possible causes of acute interstitial nephritis
- drugs (penicillin, ciprofloxacin, sulphonamides)
- infections (viral and bacterial)
possible causes of glomerular damage
- SLE (lupus, nephritis)
- rapidly progressive glomerulonephritis (GN)
- post streptococcal GN
possible causes of vascular damage
- Vasculitis, polyarteritis, nodosa
haemolytic uremic syndrome
thrombotic thrombocytopenia purport, accelerated HTN
emboli (thrombotic, atherosclerotic)
4 phases of ATN
- initiating
- oliguric
- diuretic
- recovery