Acute Kidney Injury Flashcards

1
Q

What is the KDIGO criteria for AKI?

A
  • Increase in serum creatinine >= 0.3 mg/dL
  • Increase in serum creatinine 1.5x or more than baseline of the prior 7 days
  • Urine volume < 0.5 mL/kg/h for at least 6 hours
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2
Q

which of the 3 KDIGO criteria is most often used clinically?

A

creatinine 1.5x or > than baseline of the prior 7 days

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3
Q

what are two signs that might point you towards AKI in a patient on first presentation?

A
  1. increased creatinine (however may look normal in early stages)
  2. decreased urine volume (more present in early stages)
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4
Q

define AKI

A

a sudden and often reversible reduction in kidney function

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5
Q

what is the RIFLE criteria?

A

levels of impairment
- R - risk of impairment
- I - injury to kidney
- F - kidney failure

categories of LT renal outcomes
- L - loss of kidney function over 4 wks
- E - end-stage renal disease

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6
Q

who is AKI most common in?

A

hospitalized pts in ICU

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7
Q

what is the most common cause of AKI in hospitalized pts?

A

transient renal hypoperfusion resulting in ischemic acute tubular necrosis or ischemic intrarenal AKI

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8
Q

what are some causes of prerenal AKI?

A

general: any cause of reduced blood flow to the kidney

  • Hypovolemia: diarrhea, vomiting, hemorrhage, severe burns
  • Relative fluid loss: third spacing ➔ sepsis, CHF, liver failure, anaphylaxis
  • Blockage of renal artery: renal artery stenosis, compression, blood clot
  • Medications: NSAIDs and ACEi
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9
Q

what are some causes of intrarenal AKI?

A

these are conditions that impact the glomerulus, tubules, interstitium or the vasculature

Tubular: 1) acute tubular necrosis ➔ caused by prolonged renal ischemia, sepsis, nephrotoxins; 2) intratubular obstruction ➔ casts that obstruct the tubules

Glomeruli: glomerulonephritis

interstitium: acute interstitial nephritis ➔ type I and IV hypersensitivity rxns to medications like antibiotics, NSAIDs, PPIs, and 5-ASA, autoimmune, hereditary

Vascular: microangiopathies ➔ vascular obstruction ➔ HUS, TTP, HTN emergency

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10
Q

What are some causes of postrenal aki?

A

Obstructive causes which lead to congestion and urinary backflow, usually a bilateral obstruction

obstruction: stones, neurogenic, phimosis, thrombus

compression: fecal impaction, tumours, prostate hyperplasia, retroperitoneal fibrosis, pelvic organ prolapse or masses

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11
Q

most common 3 causes of intrarenal AKI

A
  1. prolonged renal ischemia
  2. sepsis
  3. nephrotoxins
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12
Q

explain the patho for prerenal AKI

A
  1. decreased perfusion to kidney
  2. renal cell damage bc lack of O2 and nutrients from kidney hypoperfusion
  3. decreased eGFR
  4. build up of fluid/waste products in blood
  5. activation of RAAS
  6. sodium retention and water reabsorption ➔ HTN
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13
Q

would you expect urine osmolarity to be high in prerenal AKI or low? why?

A

would be high, kidney is still able to concentrate the urine and reabsorb sodium and water

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14
Q

explain the patho for intrarenal AKI

A
  1. damage to the podocytes and tubular cells ➔ increased membrane permeability and impaired reabsorption/secretion
  2. fluid overload in tubules
  3. sloughing of casts ➔ blocks tubules/obstruction
  4. overall reduced pressure difference in glomerulus and bowman’s capsule bc build of pressure
  5. not enough pressure gradient to drive filtration
  6. decreased eGFR and fluid/wastes stay in blood
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15
Q

would you expect urine osmolarity to be high in intrarenal AKI or low? why?

A

would be low, not able to concentrate urine anymore because tubules are damaged, also decreased filtration rate because less pressure difference

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16
Q

how would serum creatinine change in pre vs intra vs postrenal AKI?

A

normal/slightly high ➔ pre-renal

higher ➔ intrarenal

highest ➔ postrenal

17
Q

what are the 4 phases of AKI?

A
  1. initiation ➔ may not be symptomatic at this phase
  2. oligo-anuria ➔ reduced urine output; clinical signs usually appear at this point
  3. polyuria ➔ usually a sign that kidney is regaining function
  4. restitution/recovery
18
Q

what s/s do you expect in prerenal AKI?

A

depends on etiology
- s/s of hypervolemia from RAAS activation ➔ HTN, dyspnea, ascites, edema
- s/s of hypovolemia from etiology ➔ hypotension, syncope, ALoC, dehydration, orthostatic HTN, palpitations

19
Q

what s/s do you expect in intrarenal AKI?

A

depends on the etiology
- Autoimmune: maculopapular rashes, joint pains (lupus), oliguria
- vasculitis: purpura, bruising
- infectious: fever, chills, diaphoresis

20
Q

what s/s do you expect in postrenal AKI?

A

anuria/oliguria, dysuria/pain

21
Q

what s/s are associated with uremia/azotemia

A

rashes and itching/pruritis

may get uremic encephalopathy

22
Q

what bloodwork would you do for a suspected AKI?

A
  1. creatinine, and BUN
  2. CBC + diff
  3. electrolytes
  4. extended electrolytes
  5. ABG/VBG

bloodwork to w/u underlying etiologies
1. autoimmune markers
2. infectious causes: hepatitis, HIV, strep, blood cultures
3. toxins
4. vascular: hemolytic work up for HUS and TTP; PT/INR
5. hepatic markers: ALT/AST/ALP/GGT and albumin
6. cardiac: BNP and ECG
7. pregnancy

23
Q

what urine analysis tests do you wanna consider for AKI?

A
  1. dipstick - blood protein
  2. culture and sensitivity
  3. consider urine electrolytes
  4. specific gravity of urine
  5. urine microscopy
24
Q

what imaging would you consider for AKI?

A

KUB U/S or a CT w/o contrast

25
Q

when would you consider doing a biopsy for AKI?

A

for intrarenal cause w/ no know dx and all other tests are inconclusive

26
Q

how would you treat AKI?

A
  1. fluids!
  2. treat the underlying etiology
    - fluid overload: diuretics
    - fluid depletion: fluids
    - drug induced: stop drugs, antidote, minimize exposure
    - immune: steroids
    - infectious: abx, antiviral
    - liver: albumin, fluid management
    - electrolyte imbalances
  3. consider hemodialysis - AEIOU

would want to monitor with serial creatinine and urine output