AKI Flashcards
diagnostic criteria for AKI
Increase in SCr by >/= 0.3
increase in Scr to >/= 1.5 x baseline
urine volume <0.5 mL/kg/hr for 6 hours
what is an AKI
abrupt decline (<7 daysZ) in renal function
characterized by inability to excrete metabolic waste, maintain acid-base balance
nonoliguria
> 400 ml/day
oliguria
50-440 ml/day
anuria
<50 ml/day
measurements for AKI diagnosis
urine output
SCr (lag time 24-48 hrs behind)
4 classifications of AKI
prerenal azotemia
functional acute renal failure
acute intrinsic renal failure
post renal obstruction
what is prerenal azotemia
resulting from decreased renal perfusion
what is functional acute renal failure
decline in glomerular ultrafiltration production
what is acute intrinsic renal failure
structural damage to the kidney
what is post renal obstruction
obstruction of urine flow from the kidney
when is urine sodium concentration helpful?
to identify acute tubular necrosis from a pre-renal cause (effective volume depletion)
FENa< 1% is pre-renal cause
FENa >2% is acute tubular necrosis
how is FENa calculated
% FENa = (UNa x PCr)/(PNa x UCr) x 100
what causes pre-renal azotemia
decreased renal perfusion, hypotension
decreased blood volume
renal vessel occlusion
volume depletion
lab indicators of pre-renal azotemia
FENa< 1%
urine sodium < 20
urine osmolality > 500
what is the clinical presentation of pre-renal azotemia?
AKI hypotension present: causes decline in intravascular volume– hemorrhage, dehydration, decline in effective blood volume
can also be without hypotension
what causes functional acute renal failure
a decline in glomerular ultrafiltrate production WITHOUT DAMAGE TO THE KIDNEY. secondary to a reduced glomerular hydrostatic pressure— from changes in glomerular arteriolar circumference (vasoconstriction or vasodilation).
what are things that may cause vasoconstriction or vasodilation causing functional acute renal failure
vasoconstriction: hypocalcemia, cyclosporine, NSAIDs,, hepatorenal syndrome
vasodilation: ACEi/ARBs
what may be some causes of intrinsic renal failure
remember this is from DAMAGE to the kidney: may be from
-acute tubular necrosis (toxin exposure- contrast dye)
-ischemia (hypotension, pressors)
-Acute interstitial nephritis
-tubular damage
-small vessel disease
what is the clinical presentation of intrinsic AKI?
urine osmolality <250
urine sodium >20
FENa>1%
what are the medications causing intrinsic renal failure
antibiotics
anticonvulsants
loop diuretics
NSAIDs
structural areas of the kidney for potential damage in intrinsic renal failure
vasculature (small blood vessels)
glomeruli
renal tubules
interstitium
what is VASCULAR intrinsic renal failure
occlusion of a part of the vasculature that supplies the kidney with oxygenated blood.
can be caused by thrombotic emboli
what is acute tubular necrosis
death of tubular cells that form the tubule that transports urine to the ureters
causes muddy brown casts in the urine
FENa in ATN
usually >3%
what is GLOMERULUS intrinsic renal failure
inflammation of the glomeruli (caused by lupus, poststreptococcal infection, hepatitis C, etc) which is the 3rd most common cause of renal disease behind diabetes & HTN
difference between toxic ATN and ischemic ATN
toxic: characterized by proximal tubular epithelium necrosis due to a toxic substance (caused by meds like aminoglycosides, amphotericin B, cisplatin, contrast)
ischemic: caused when kidneys are not sufficiently perfused for a long period of time, or during shock
what is INTERSTITIUM intrinsic renal failure
interstitium provides the structural support, environment to establish concentration gradients
caused by infection in the kidneys (pyelonephritis) or medication reaction (PCN, Ceph, NSAIDs)
______ must involve both kidneys for injury
post renal obstruction
(remember this is obstruction of urine flow from the kidney)
causes of post renal obstruction
bladder outlet obstruction (prostate hypertrophy)
crystal deposits in the tubules (uric acid, methotrexate, acyclovir)
urethral obstruction
commonly implicated agents in drug induced AKI
antimicrobials (aminoglycosides, acyclovir, amphotericin)
chemo (cisplatin, cyclophosphamide)
calcineurin inhibitors (cyclosporine, tacrolimus)
NSAIDs
IV contrast
what are some possible MECHANISMS for drug induced AKI
direct renal toxicity (aminoglycosides, cisplatin, amphotericin)
crystallization/obstruction (acyclovir, ganciclovir, methotrexate)
reduction in glomerular blood flow (NSAID, ACEi, ARB)
what to do if a nephrotoxic drug is needed?
utilize renal-protective therapies
ensure patient is not dehydrated prior to nephrotoxic medication administration
what is the diagnosis when there are muddy brown casts
ATN
what is the diagnosis when urinalysis shows + hemoglobin without RBC
rhabdomyolysis
what is the diagnosis when urinalysis shows WBCs, bacteria, nitrates; and microscope findings are WBC casts
pyelonephritis
what is the diagnosis when urinalysis shows WBCs and no bacteria, proteinuria, hematuria
Acute interstitial nephritis
what is the diagnosis when urinalysis shows hematuria, proteinuria. microscope shows RBC casts, dysmorphic RBC
glomerulonephritis
possible treatments for AKI
remove the offending agent/correct underlying cause
avoid nephrotoxic agent
fluid bolus if prerenal cause
possibly diuretics
dialysis (AEIOU)
don’t recommend dopamine receptor agonists
what are some alternative drugs to the commonly nephrotoxic drugs
lipid based ampho b vs conventional
extended interval aminoglycoside dosing vs traditional
low osmolality contrast medium vs higher osmolality dyes
acetaminophen vs nsaids
how to treat if prerenal cause (FENa<1%)
fluid bolus of a crytalloid; rapid fluid resuscitation can improve renal perfusion and rescue hypoxic tubules
______ test is helpful to see if fluid resuscitation is beneficial
furosemide
who to trial furosemide test?
patients thought to be fully resuscitated
persistent oliguria (50-440)
clinicians unsure what would help
what if outcome of furosemide test is urine output >200 mL in 2 hours?
pre-renal oliguria: replace output with IV crystalloid; attempt hemodynamic strategy to improve urine output
what if outcome of furosemide test is urine output <200 mL in 2 hours?
intrinsic kidney failure; more fluid, pressors, or inotropes are unlikely to help.
t/f: diuretics speed up recovery and improve prognosis
false
when are diuretics useful
fluid management (pulmonary edema, reduce need for dialysis, increase K elimination)
diuretic strategies
furosemide 80 mg IV x 1: if no increase in urine output, can double.
can also try continuous infusion of loops instead of intermittent.
can also try synergy with thiazide + loop (thiazides aren’t useful as monotherapy)
mannitol: use caution, hyperosmolar result
____ are paired for additive effect with loop diuretics but are not useful as monotherapy in AKI
thiazide diuretics
dopamine and fenoldopam for AKI
don’t recommend
indications for dialysis
AEIOU
Acid base
Electrolyte imbalance
Intoxication
Overload (of fluid)
Uremia
major disadvantage of hemodialysis
hypotension
(not tolerated in the hemodynamically unstable)
advantages/disadvantages of CRRT
advantage: continuous removal, better tolerated
disadvantage: nursing time, DOSING SUCKS
AKI results in _____ clearance of renally eliminated drugs
decreased
with iHD, when to administer drugs?
after session
3 common causes of AKI in the ICU
sepsis
rhabdomyolysis
drug induced
why does sepsis cause AKI
hypotension: causes decreased renal perfusion
treating sepsis/AKI
immediate administration of antibiotics is necessary; renal dose adjustments must be made
rhabdomyolysis is characterized by
leakage of muscle-cell contents (electrolytes, myoglobin) into the circulation.
patient will present with pigmented granular casts, reddish-brown urine supernatant, rased CPK >20,000
what are common causes of rhabdomyolysis in ICU
trauma (crush)
muscle hypoxia (person found down, limb compression during prolonged loss of consciousness)
drugs/toxins (statins, fibrates, alcohol, heroin, cocaine, daptomycin)
infections (viral, bacterial)
why is there AKI in rhabdomyolysis
myoglobin is released from muscle
iron released from myoglobin generates ROS which damages the kidney
AND blood flow is decreased to the kidney
treating rhabdomyolysis/AKI
if a drug is involved, d/c it.
adequate fluid hydration starting with 1-2 L of fluid/hr and goal urine output is 200-300 mL/hr
raise urine pH>6.5 (urine alkalinization prevents heme-protein precipitation) with sodium bicarbonate
maybe dialysis
what are some preventative strategies prior to nephrotoxins???
hydration of sodium loading
0.9% NaCl most effective
1-2 mL/kg/hr starting 4 hours before nephrotoxin
goal urine output is at least 0.5 mL/kg/hr
who gets prophylaxis for contrast dye
patients with high risk: AKI, GFR<30 and not on dialysis
what is prophylaxis regimen for contrast induced nephropathy
0.9% NS 1 mL/kg/hr for 6-12 hrs PREPROCEDURAL
1 mL/kg/hr during and 6-12 hrs POSTPROCEDURAL
