Acute Kidney Injury Flashcards
contrast media assoc with lower incidence of aki
Low osmolar, isosmolar
acute decline in gfr in cin occurs in ___ and peak crea concentration in ____
24 to 48 hours
3 to 5 days
most nephrotoxic amino glycosides
neomycin
kidney hypoperfusion resulting from reductions in actual or effective arterial blood volume
prerenal AKI
autoregulation works only to a mean sytemic MAP of
75 to 80 mmHg
idiosyncratic allergic response to different pharmacologic agents
Acute interstitial nephritis
hallmark of AIN
inflammatory infiltrates within the interstititium
2nd most common cause of intrinsic AKI
nephrotoxic ATN
pathophysiology of CIN
(3)
hypoxic and renal tubular damage +
endothelial dysfunction +
altered microcirculation
to limit cast formation and preventive measure in tubular disease with endogenous nephrotoxins
(2)
volume expansion, alkalinization of urine
what will accelerate and aggravate light chain cast nephropathy
reduction in GFR
most common cause for post renal azotemia
structural or functional obstruction of the bladder neck
major and most commonly injured epithelial cell involved in AKI related to ischemia, sepsis and or nephrotoxins
proximal tubular cell
most susceptible to ischemic injury
S3 proximal tubule in the outer stripe of the medulla
primarily responsible for the extension phase of AKI
endothelial cell injury and dysfunction
passive non-energy dependent process that develops secondary to severe ATP depletion from toxic or ischemic insult
epithelial cell necrosis
form of regulated nonapoptotic cell death in ischemic/cisplatin induced AKI
necroptosis
Folic acid induced AKI
ferroptosis
highly inflammatory form of regulated cell death
pyroptosis
facilitate the restoration of normal function by assisting in the refolding of denatured proteins/appropriate folding of newly synthesized proteins
heat shock proteins
significant reduction in blood vessel density after ischemic injury
vascular dropout
One of the major risk factors for the development of dialysis requiring AKI
Preexisting kidney disease
iodinated contrast agents
prerenal acute kidney injury
history of atrial fibrillation or recent MI, nausea, vomiting, flank or abdominal pain; mild proteinuria occasional rbcs; elevated LDH, normal transaminase levels
renal artery thrombosis
recent manipulation of aorta, retinal plaques, subcutaneous nodules, purpura, livedo reticularis; eosinophiluria; eosinophilia, hypocomplementemia
atheroembolism
nephrotic syndrome; pulmonary embolism; flank pain; proteinuria, hematuria
Renal vein thrombosis
typical urinalysis findings in HUS/TTP (3)
RBCs, mild proteinuria, rarely RBC or granular casts
urine findings in rhabdomyolysis, hyperK, hyperphos, hypocalcemia, increased CK, myoglobin
positive for heme in absence of RBCs
urine findings in hemolysis, hyperK, hyperphos, hypocal, hyperuricemia and free circulating hgb
pink and positive for heme in absence of RBCs
urine findings in tumor lysis, myeloma, ethylene glycol(3)
urate crystals, dipstick proteinuria, oxalate crystals
calcium oxalate crystals
ethylene glycol intoxication
lafbp is detected in the urine within how many hours to ischemic or nephrotoxic injury
6 hours
mL of post void residual volume indicative of bladder outlet obstruction
100-150 ml
Cairo Bishop definition of tumor lysis syndrome
(4)
2 of the following achieved in the same 24h interval from 3 days before to 7 days after chemo:
uric acid > 8,
K >6,
phos > 4.6,
calcium < 7 mg/dL
Diagnostic criteria for HRS (5)
- cirrhosis with ascites
- AKI
- no improvement of AKI after 2 days of diuretic withdrawal and volume expansion
- absence of shock
- absence of parenchymal kidney disease
definitive therapy for abdominal compartment syndrome
surgical laparotomy
at risk hospitalized patients for contrast associated AKI rate of isotonic sodium chloride
1 ml/kg per hr for 6-12 hours prior and after procedure
at risk outpatients for contrast associated AKI, rate of isotonic sodium chloride
3 ml/kg 1 hour prior to procedure then 6 ml/kg per hr over 2-6 hours after procedure
used to limit uric acid generation with acute urate nephropathy
allopurinol 100 mg/m2 every 8 hours (max 800 mg/day)
effective prophylaxis and treatment for acute uric acid mediated tumor lysis syndrome
rasburicase
corticosteroids in AIN if considered dose
Methlypred 250-500 mg/day for 3-4 days then oral pred 1 mkd over 8-12 weeks
if the duration of AKI is short, not extremely catabolic and does not require RRT; dietary protein requirement is
0.8-1 g/kg bw/day
If duration of AKI is prolonged, with hypercatabolism or on RRT, dietary protein intake
1-1.5 kg/bw/day
total caloric intake with prolonged AKI
20-30 kcal/kg/by/day
transfusion threshold
7 g/dL
Kt/V recommended for RRT in AKI
3.9/week
effluent volume during CRRT
20-25 ml/kg/hr
FeNa in Radio Contrast Induced Nephrotoxicity
<1%
AKI resolves within
1-2 weeks
biomarker of AKI associated with reducing apoptosis and enhancing normal proliferation of renal tubular cells
NGAL
Diagnosis of Clinical Tumor lysis syndrome
laboratory + at least one of the ff: 1. Crea more than 1.5x, cardiac arrhythmia/sudden death, seizure
acute worsening of heart function leads to AKI
Acute CRS Type 1
chronic abnormalities in heart function result in kidney dysfunction
Chronic CRS Type 2
AKI precedes cardiac dysfunction
Acute renocardiac (Type 3)
CKD leads to cardiac dysfunction
Chronic renocardiac (Type 4)
Systemic conditions result in simultaneous cardiac and renal dysfunction
secondary CRS (Type 5)
rapid progressive AKI with doubling of the serum crea to > 2.5 in < 2 weeks
Type 1 HRS
Moderate renal dysfunction (Crea 1.5-2.5) with steady or slowly progressive course
Type 2 HRS
initial management of volume resuscitation
isotonic saline 0.9%
amount of albumin per Liter of ascites drained when paracentesis volume exceeds 5L
6 to 8 g albumin
vasoconstrictive agent combined with volume expansion that may improve kidney function in hrs
terlipressin
Early Goal Directed therapy for sepsis(4)
MAP > 65,
CVP 10-12,
UO > 0.5 ml/kg/hr,
CVO2 > 70%
Relative indications for RRT in AKI
progressive azotemia without uremic manifestations, persisitent oliguria
cardinal manifestation of AKI
decreased urine output
nonoliguric uo
uo > 400 ml/day
oliguric uo
UO < 400 ml/day
anuric
uo < 100 ml/day
AKI RIFLE
increase of > 50% developing over 7 days
AKI AKIN (2)
Increase of > 0.3 mg/dL or
> 50% developing over < 48 hours
KDIGO AKI (2)
Increase of > 0.3 mg/dL over <48 hours or
an inc of > 50% developing over < 7 days
urine output in AKI definition
< 0.5 ml/kg/hr for > 6 hours
More than 50% (> 0.3 mg/dL) increase in crea stage
Risk, Stage 1
More than 100% increase in crea stage
Injury, Stage 2
More than 200% increase in crea stage
Failure Stage 3
need for RRT for >4 weeks stage of AKI
Loss
need for RRT for > 3 months stage of AKI
End Stage
UO in Risk or Stage 1 AKI
< 0.5 ml/kg/h for > 6 h
UO in Injury or Stage 2 AKI
< 0.5 ml/kg/h for > 12 h
UO in Failure or Stage 3 AKI
< 0.3 ml/kg/h for ? 24h or anuria for >12 h
most common cause of AKI
prerenal
hallmark feature in ATN
loss of the apical brush border of PTC
FeNa in ATN
> 2
UNa in Prerenal vs ATN
<20 vs >40
Urine-Plasma Crea ratio Prerenal vs ATN
> 40 vs < 20
UOsm prerenal vs ATN
> 500 vs 300
Plasma BCr (pre renal vs renal)
> 20 vs <10-15
organic thiophosphate to ameliorate cisplatin toxicity
Amifostine
limits acetaminophen induced renal injury if given within 24H of ingestion
NAC
Chelating agent that may prevent heavy metal nephrotoxicity
Dimercaprol
inhibits ethylene glycol metabolism to oxalic acid
Ethanol
inhibitor of alcohol dehydrogenase that decreases production of ethylene glycol metabolites
Fomepizole
