Acute Kidney Injury Flashcards by Stephanie Floyd

contrast media assoc with lower incidence of aki

Low osmolar, isosmolar

How well did you know this?

Not at all

Perfectly

acute decline in gfr in cin occurs in ___ and peak crea concentration in ____

24 to 48 hours

3 to 5 days

How well did you know this?

Not at all

Perfectly

most nephrotoxic amino glycosides

neomycin

How well did you know this?

Not at all

Perfectly

kidney hypoperfusion resulting from reductions in actual or effective arterial blood volume

prerenal AKI

How well did you know this?

Not at all

Perfectly

autoregulation works only to a mean sytemic MAP of

75 to 80 mmHg

How well did you know this?

Not at all

Perfectly

idiosyncratic allergic response to different pharmacologic agents

Acute interstitial nephritis

How well did you know this?

Not at all

Perfectly

hallmark of AIN

inflammatory infiltrates within the interstititium

How well did you know this?

Not at all

Perfectly

2nd most common cause of intrinsic AKI

nephrotoxic ATN

How well did you know this?

Not at all

Perfectly

pathophysiology of CIN
(3)

hypoxic and renal tubular damage +
endothelial dysfunction +
altered microcirculation

How well did you know this?

Not at all

Perfectly

to limit cast formation and preventive measure in tubular disease with endogenous nephrotoxins
(2)

volume expansion, alkalinization of urine

How well did you know this?

Not at all

Perfectly

what will accelerate and aggravate light chain cast nephropathy

reduction in GFR

How well did you know this?

Not at all

Perfectly

most common cause for post renal azotemia

structural or functional obstruction of the bladder neck

How well did you know this?

Not at all

Perfectly

major and most commonly injured epithelial cell involved in AKI related to ischemia, sepsis and or nephrotoxins

proximal tubular cell

How well did you know this?

Not at all

Perfectly

most susceptible to ischemic injury

S3 proximal tubule in the outer stripe of the medulla

How well did you know this?

Not at all

Perfectly

primarily responsible for the extension phase of AKI

endothelial cell injury and dysfunction

How well did you know this?

Not at all

Perfectly

passive non-energy dependent process that develops secondary to severe ATP depletion from toxic or ischemic insult

epithelial cell necrosis

How well did you know this?

Not at all

Perfectly

form of regulated nonapoptotic cell death in ischemic/cisplatin induced AKI

necroptosis

How well did you know this?

Not at all

Perfectly

Folic acid induced AKI

ferroptosis

How well did you know this?

Not at all

Perfectly

highly inflammatory form of regulated cell death

pyroptosis

How well did you know this?

Not at all

Perfectly

facilitate the restoration of normal function by assisting in the refolding of denatured proteins/appropriate folding of newly synthesized proteins

heat shock proteins

How well did you know this?

Not at all

Perfectly

significant reduction in blood vessel density after ischemic injury

vascular dropout

How well did you know this?

Not at all

Perfectly

One of the major risk factors for the development of dialysis requiring AKI

Preexisting kidney disease

How well did you know this?

Not at all

Perfectly

iodinated contrast agents

prerenal acute kidney injury

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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)

1. cirrhosis with ascites 2. AKI 3. no improvement of AKI after 2 days of diuretic withdrawal and volume expansion 4. absence of shock 5. 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

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