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renal > acute kidney injury > Flashcards

acute kidney injury Flashcards

1
Q

AKI definition

A

a sudden decline in renal function over hours to days

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2
Q

non-oliguric

A

urine output is >400c/day

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3
Q

oliguric

A

urine output is <400 cc/day

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4
Q

anuric

A

urine output is <100cc/day

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5
Q

which group tends to have the highest rate of AKI

A

pts in the ICU, 50% have AKI

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6
Q

what does RIFLE stand for

A

risk, injury, failure, loss, end-stage kidney disease

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7
Q

what is RIFLE?

A

a classification system for AKI based on GFR and urine output

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8
Q

what is AKIN?

A

AKI network

classification for AKI based on Scr and urine output

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9
Q

What is KDIGO used for?

A

it is a staging system that is based on Scr and urine output

stages correlate with the risk of death and long-term outcomes

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10
Q

AKI stage 1 KDIGO

A

increase in SCr > 0.3 in 48 hrs OR
increase in SCr >1.5x baseline OR
urine volume < 0.5 ml/kg/hr x 6 hrs

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11
Q

3 main types of AKI

A

pre-renal
post renal
intrinsic renal

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12
Q

pre-renal AKI

A

any condition that leads to decreased renal perfusion

60% of cases of AKI

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13
Q

pre-renal AKI pathophys

A

decreased perfusion activates RAAS.

release of renin then releases ADH= vessel contraction to preserve blood flow to heart and brain

=decreased GFR so kidneys respond by concentrating urine and holding onto Na to try and reabsorb water

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14
Q

causes of pre-renal AKI

A

decreased volume (GI losses, hypovolemia)
decreased effective volume (cirrhosis, CHF)
Rx (ACE/ARBs, NSAIDs)

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15
Q

cardiorenal syndrome

A

cause of pre-renal AKI that results from decreased cardiac performance leading to decreased cardiac output which leads to decreased renal perfusion and increased water and Na retention (hypervolemia)

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16
Q

hepatorenal syndrome

A

consequence of cirrhosis that causes pre-renal AKI due to decreased renal blood flow

most likely due to portal hypertension leading to decreased GFR

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17
Q

clinical presentation of pre-renal AKI

A

signs of volume depletion
orthostatic hypotension
reduced skin turgor, dry mucous membranes
ascites, edema
(history is essential for revealing cause)

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18
Q

pre-renal AKI diagnostic findings

A

FeNA <1%
BUN:Cr ratio > 20:1
urine Na <20

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19
Q

how do you determine the mechanism of AKI?

A

clinical presentation, history, response to therapy

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20
Q

pre-renal AKI treatment

A

supportive care
fluid repletion with normal saline or LR
treat underlying cause (blood transfusions, hold rx that can contribute)

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21
Q

you would give ____ for hypovolemia and ___ for hypervolemia

A

IV fluids

diuretics

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22
Q

what is FeNA?

A

fractional excretion of Na, used to distinguish pre-renal AKI from ATN
FeNA<1= pre-renal AKI
FeNA > 2= acute tubular necrosis

*may not be accurate

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23
Q

pre-renal AKI response to treatment

A

rapid improvement in renal function following acute intervention

24
Q

intrinsic AKI

A

AKI that leads to severe direct kidney damage

~35% of cases of AKI

25
Q

types of intrinsic renal injury

A

tubular
interstitial
glomerular
vascular

26
Q

acute tubular injury

A

causes 85% of intrinsic AKIs

can be ischemic or nephrotoxic (from drugs)

27
Q

ischemic ATI pathophys

A

severe decrease in renal blood flow leads to tubular cell injury and inflammation secondarily, which ultimately results in necrosis of cells and impaired reabsorption

28
Q

toxic ATI pathophys

A

injury occurs to tubular cells directly due to nephrotoxic substances leading to decreased GFR

29
Q

ATI diagnosis

A

history: is there event that may have caused it?
FeNa>2, progressive rise in Cr
urinalysis shows muddy brown granular epithelial casts
lack of improvement in Cr with IV fluids

30
Q

what is a difference between ATI and prerenal AKI based on Cr?

A

prerenal AKI BUN:Cr = >20:1
ATI= <15:1
there is a lack of improvement in Cr with IV fluids in ATI, prerenal Cr improves with repletion

31
Q

ATI treatment

A

supportive care
remove nephrotoxic offending agents
carefully balance fluid and electrolytes without overloading (depends on urine output)

32
Q

acute glomerulonephritis

A

intrinsic cause of AKI that is the inflammation and damage of the glomeruli

33
Q

acute GN diagnosis

A

urinalysis with protein, blood, WBC, RBC cases

evidence of other systemic disease

**renal biopsy to find out cause

34
Q

acute interstitial damage

A

acute inflammation of renal tubules and interstitial that can cause intrinsic AKI

35
Q

acute interstitial damage pathophysiology

A

hypersensitivity reaction usually to drugs or infection that causes inflammation and damage to the interstitial fluid

36
Q

drugs that can cause acute interstitial damage

A 
abx
PPIs
cephalosporins
sulfonamides
penicillin
NSAIDs
37
Q

acute interstitial damage physical exam

A

rash, fever, CVA tenderness

38
Q

acute interstitial damage diagnosis

A

urinalysis with WBC casts
PBS shows eosinophilia
renal biopsy shows interstitial T-cell and monocyte infiltration

39
Q

acute interstitial damage treatment

A

stop the offending rx that is causing reaction (no shit)

steroids, IV fluids

40
Q

what can vascular injury cause and how?

A

can cause intrinsic AKI due to injury to the infrarenal vessels

41
Q

main types of rx that can lead to nephrotoxicity

A

antibiotics, acyclovir, amphotericin b, MTX, cisplatin, NSAIDs, cyclosporine, iodine and gadolinium contrast

42
Q

causes of vascular injury

A

HUS, TTP, malignant HTN, vasculitis, atheroembolic disease

43
Q

physical exam findings of vascular injury

A

petechiae, purpura, livedo reticularis, thromboemboli

44
Q

vascular injury diagnosis and treatment

A

renal US

treatment to get rid of clot-angioplasty, endovascular tx, thrombolytics

45
Q

post-renal AKI pathophys

A

acute bilateral urinary flow obstruction leads to increase in intratubular pressure and causes decrease in GFR, can also lead to impaired renal blood flow

46
Q

causes of post-renal AKI

A

BPH, stones, tumors, neurogenic bladder, iatrogenic like from catheter injury

anything that causes bilateral obstruction of urinary flow

47
Q

post renal AKI clinical presentation

A
  • decreased or no urine output
  • infection or UTI due to obstruction
  • flank pain if due to stones
48
Q

post-renal AKI diagnosis

A

renal US or CT scan of abdomen/pelvis showing bladder distention, high postpaid residual volume, stones

49
Q

post-renal AKI tx

A

relieve obstruction

  • stents for stones
  • catheterization
  • rx for BPH
50
Q

one word for the cause of pre-renal AKI

A

hypoperfusion

51
Q

two words for the cause of intrinsic AKI

A

parenchymal damage

52
Q

one word for the cause of post-renal AKI

A

obstruction

53
Q

hemodynamic support for AKI pt who is hypovolemic

A

IV fluid resuscitation

consider pressors if pt is very hypotensive

54
Q

hemodynamic support for AKI pt who is hypervolemic

A

fluid restriction

consider loop diuretics if pt is volume overloaded

55
Q

hemodynamic support for AKI pt who is euvolemic or unknown volume status

A

try administering a small amount of IV fluid and seeing if pt is responsive

56
Q

most widely used classification system for AKI

A

KDIGO- based on SCr and urine output

renal (17 decks)

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