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
What type of aki
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
Intoxication from what would cause
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