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PTP&M: Nephro > AKI (Acute Kidney Injury) > Flashcards

AKI (Acute Kidney Injury) Flashcards

1
Q

3 Defining Characteristics: AKI

A
  1. ) Rapid decline in GFR
  2. ) Fluid, electrolyte, acid/base disruption
  3. ) Nitrogenous waste accumulation (azotemia)
    * *azotemia: LOOK AT BUN
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2
Q

KDIGO: AKI Definition

A
  1. ) Increase SCr ≥ 0.3mg/dL in 48hr from baseline
  2. ) Increase SCr ≥1.5mg/dL in 7d from baseline
  3. ) Urine volume ≤0.5mL/kg/hr for 6hr
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3
Q

Azotemia

A

Increase in BUN and SCr

*seen in a blood test (typically)

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4
Q

Uremia

A

Azotemia + Clinical S/Sx

  1. ) N/V
  2. ) Decreased platelet aggregation (“uremic bleeding”)
  3. ) Encephalopathy
  4. ) Pericardial effusion
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5
Q

Output Definition: Anuria

A
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6
Q

Output Definition: Oligonuria

A

≤500mL/day

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7
Q

Output Definition: Non-oligonuria

A

> 500mL/day

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8
Q

AKI Classifications (3)

A

RIFLE (Risk, Injury, Failure, Loss, ESKD)
AKIN (Stage 1-3)
KDIGO (Stage 1-3)

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9
Q

RIFLE Category Criteria: R

A

R = Risk
SCr Criteria:
Increase 1.5x from baseline OR >25% GFR DECLINE from baseline

Urine Criteria:

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10
Q

RIFLE Category Criteria: I

A

I = Injury
SCr Criteria:
Increase 1-2x OR >50% GFR DECLINE from baseline
Urine Criteria:

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11
Q

RIFLE Category Criteria: F

A 
F = Failure
SCr Criteria: 
SCr increase 3x   OR   GFR DECLINE >75% from baseline  OR SCr ≥4mg/dL with acute increase ≥0.5mg/dL
Urine Criteria:
ANURIA ≥ 12hr
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12
Q

RIFLE Category Criteria: L

A 
L = Loss
SCr Criteria: 
Complete loss of Fx
Urine Criteria:
N/A
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13
Q

RIFLE Category Criteria: E

A 
E = ESKD
SCr Criteria: 
RRT > 3months  (renal replacement therapy)
Urine Criteria:
N/A
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14
Q

AKIN: General Characteristics (3)

A
  1. ) Defines AKI as “abrupt decrease in kidney Fx” (≤48hr)
  2. ) NO GFR calculation included in staging
  3. ) FLE (from RIFLE) included in AKIN Stage 3
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15
Q

AKIN: Stage 1

A

SCr Criteria:
SCr ≥ 0.3mg/dL OR 1.5-2x from baseline
Urine Criteria:

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16
Q

AKIN: Stage 2

A

SCr Criteria:
2-3x increase from baseline
Urine Criteria:

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17
Q

AKIN: Stage 3

A

SCr Criteria:
>3x increase from baseline OR ≥4mg/dL with acute increase of ≥0.5mg/dL, or RRT
Urine Criteria:

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18
Q

KDIGO: Stage 1

A

SCr Criteria:
Increase ≥0.3mg/dL or 1.5-1.9x from baseline
Urine Criteria:

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19
Q

KDIGO: Stage 2

A

SCr Criteria:
Increase 2-2.9x from baseline
Urine Criteria:
0.5mL/kg/hr ≥12hr

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20
Q

KDIGO: Stage 3

A

SCr Criteria:

SCr increase 3x from baseline, or SCr ≥4mg/dL, or need of RRT, or eGFR

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21
Q

AKI: General Management (7)

A
  1. ) Hemodynamic Stability
  2. ) Fluid Management
  3. ) Electrolyte management
  4. ) Renal perfusion
  5. ) Hydration
  6. ) Eliminate nephrotoxins (if possible)
  7. ) Renal Replacement Therapy (RRT)
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22
Q

KDIGO: AKI Stage 1

A
  1. ) Non-invasive diagnostic workup

2. ) Consider invasive diagnostic workup

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23
Q

KDIGO: AKI Stage 2

A

Stage 1+

  1. ) Check for drug-dosing changes
  2. ) Consider RRT
  3. ) Consider ICU admission
24
Q

KDIGO: AKI Stage 3

A

Stage 1 ,2 +:

Avoid subclavian catheters (if possible)

25
Q

AKI Types + Mortality Rates (3)

A

Community-acquired AKI (n/a)
Hospital-acquired AKI (15-40%)
ICU-acquired AKI (30-90%)

26
Q

CA-AKI: Risk Factors (5)

A
  1. ) Chronic co-morbid conditions
  2. ) Elderly
  3. ) Male
  4. ) Sepsis/infection
  5. ) Drugs (ACEi, arbs, diuretics)
27
Q

HA-AKI: Risk Factors (6)

A
  1. ) Volume depletion
  2. ) Hypotension
  3. ) Sepsis
  4. ) Low cardiac output
  5. ) Nephrotoxic drugs
  6. ) Radiocontrast dyes
28
Q

ICU-AKI: Risk Factors (6)

A
  1. ) Septic shock
  2. ) Major surgery
  3. ) Multi-organ failure
  4. ) Hypotension
  5. ) Low cardiac output
  6. ) Nephrotoxic drugs
29
Q

AKI Etiologies (3)

A
  1. ) Pre-renal (glomerulus, arterioles) 70% Cases
  2. ) Intrinsic (PCT, LH, DCT, CT(s)) 25% Cases
  3. ) Post-renal (bladder, ureter) 5% Cases
30
Q

Post-Renal AKI: Causes (2)

A

Bladder outlet obstruction

Ureteral obstruction

31
Q

Post-Renal AKI: Labs + Urinalysis (4)

A
  1. ) BUN : SCr ~ 15
  2. ) Urine cellular debris
  3. ) Urine : serum osmolality
32
Q

FeNa: Equation

A

Fractional Excretion of Sodium (limited usefulness with diuretics)

100 x [(Urine sodium x SCr) / ( Urine creatnine x Serum sodium)]

33
Q

Post-Renal AKI: Management

A
  1. ) Obstruction removal
  2. ) Alpha-1 blockers (BPH)
  3. ) Catheterization
  4. ) Percutaneous nephrostomy
34
Q

Pre-Renal AKI: Causes

A
  1. ) Hypoperfusion
  2. ) Volume depletion (hemorrhage, vasodilation (sepsis), diuretics, nephrotic syndrome/cirrhosis)
  3. ) Decreased CO (cHF, MI, PE)
  4. ) Fx changes (reduced intraglom. pressure)
35
Q

Pre-Renal AKI: Clinical Features

A
  1. ) Volume depletion evidence
    * thirst, hypotension, tachycardia
  2. ) Decreased perfusion volume evidence
    * ascites, edema
  3. ) Severe infection
    * fever, hypotension, blood culture +
  4. ) Nephro-toxic drugs (NSAIDs, ACEi, diuretics)
36
Q

Renal Dynamics + ACEi Effects

A

Prostaglandins/COXs vasodilate AFFERENT
Angiotensin II constricts EFFERENT arteriole
Drop in intraglomerular pressure due to ACE inhibition

37
Q

Pre-Renal AKI: Labs + Urinalysis (4)

A
  1. ) Normal urine sediment (NO CASTS)
  2. ) Urine:Serum osmolality > 1.5
  3. ) BUN : SCr > 20
  4. ) Low FeNa (
38
Q

Pre-Renal AKI: Management (4)

A
  1. ) Restore renal blood flow by increasing intravascular volume
  2. ) Hemorrhage –> packed RBCs
  3. ) Plasma loss (burns) –> NS
  4. ) Increase CO –> positive ionotropes, intra-aortic balloon pump
39
Q

Intrinsic AKI

A

Intra-kidney damage

  • vascularture
  • glomerulus
  • tubules
  • interstitium
40
Q

Intrinsic AKI: DI Causes

A
  1. ) Glomerulonephritis (NSAIDs)
  2. ) Hemolytic uremic snydrome/TTP (clopidogrel)
  3. ) Allergic interstitial nephritis (ABXs)
41
Q

Intrinsic AKI: Tubular Damage

A

MAJORITY OF CASES (85%)

  • 50% –> pre-renal ischemia
  • 35% –> direct tubular toxins
42
Q

Intrinsic AKI: Causes + Drugs (6)

A
  1. ) ACUTE TUBULAR NECROSIS (ATN)
    * post prerenal ischemic insult
  2. ) Nephrotoxins (radiocontrast dyes, aminoglycosides (STAG), etc.)
  3. ) Rhabdomyolysis (statins)
  4. ) Hemolysis (carbidopa)
  5. ) Tumor Lysis Syndrome (chemotherapy)
  6. ) Ethylene glycol/methanol ingestion
43
Q

Post-Ischemic ATN: Pathophys

A

Prolonged Ischemia resulting in renal damage (parenchyma)

Severe renal hypoperfusion may result in permanent failure

44
Q

Post-Ischemic ATN: Phases

A

S/Sx similar to prerenal failure (does NOT resolve with fluid replacement therapy)

  1. ) Oliguric/initiation
  2. ) Diuretic/maintenance
  3. ) Recovery
45
Q

Phases of ATN: Oliguric/Initiation Phase

A

1-2 Week Duration

  • tubular cell death
  • diminshed urine output (
46
Q

Phases of ATN: Diuretic/maintenance

A
  • Indicates initial kidney recovery
  • increased urine output
  • GFR increases gradually
  • Na reabsorption/urine concentration increases
47
Q

Phases of ATN: Recovery

A
  • azotemia (5-60d resolution)
  • urine concentration within months
  • 90-95% GFR return to baseline
  • 50% return of baseline (if initial baseline is poor)
48
Q

Post-Ischemic ATN: Labs/urinalysis

A
  1. ) Muddy brown urine
  2. ) Granular/epithelial cell casts
  3. ) U/S osmolality 2%
  4. ) High [Mg++] + tubular enzymes
49
Q

Post-Ischemic ATN: Management

A

Improve urine output
Restore kidney Fx
Decrease need for RRT
Improved survival

50
Q

AKI: Complications

A
  1. ) Volume overload
  2. ) Edema
  3. ) Metabolic acidosis
  4. ) Malnutrition
  5. ) Drug-adjustments
51
Q

Volume Overload: Management

A
  1. ) Fluid restriction
  2. ) Diuretics
  3. ) Limit Na-intake (DASH diet)
  4. ) Dopamine
52
Q

PK: Loop Diuretics

A

Furosemide (2-2.5hr) RENAL ELIMINATION
glucouronidated
Bumetanide (2-2.5hr) HEPATIC ELIMINATION (P450)
Torsemide (6hr) HEPATIC ELIMINATION (P450)

53
Q

Ceiling Dose: Furosemide

A

IV: 160-200mg (q6h)
PO: >200mg (?)

54
Q

Ceiling Dose: Bumetanide

A

IV: 8-10mg (q6h)
PO: 8-10mg (QD)

55
Q

Ceiling Dose: Torsemide

A

IV: 50-100mg (q12h)
PO: 50-100mg (QD)

56
Q

TZD Synergy Doses (2 Rx)

A

HCTZ (CrCl-based):
> 50mL/min —> 25-50mg QD
25-50mL/min –> 50-100mg QD
100-200mg/day

Metolazone
5-10mg QD

PTP&M: Nephro (6 decks)

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