AKI (Acute Kidney Injury) Flashcards
1
Q
3 Defining Characteristics: AKI
A
- ) Rapid decline in GFR
- ) Fluid, electrolyte, acid/base disruption
- ) Nitrogenous waste accumulation (azotemia)
* *azotemia: LOOK AT BUN
2
Q
KDIGO: AKI Definition
A
- ) Increase SCr ≥ 0.3mg/dL in 48hr from baseline
- ) Increase SCr ≥1.5mg/dL in 7d from baseline
- ) Urine volume ≤0.5mL/kg/hr for 6hr
3
Q
Azotemia
A
Increase in BUN and SCr
*seen in a blood test (typically)
4
Q
Uremia
A
Azotemia + Clinical S/Sx
- ) N/V
- ) Decreased platelet aggregation (“uremic bleeding”)
- ) Encephalopathy
- ) Pericardial effusion
5
Q
Output Definition: Anuria
A
6
Q
Output Definition: Oligonuria
A
≤500mL/day
7
Q
Output Definition: Non-oligonuria
A
> 500mL/day
8
Q
AKI Classifications (3)
A
RIFLE (Risk, Injury, Failure, Loss, ESKD)
AKIN (Stage 1-3)
KDIGO (Stage 1-3)
9
Q
RIFLE Category Criteria: R
A
R = Risk
SCr Criteria:
Increase 1.5x from baseline OR >25% GFR DECLINE from baseline
Urine Criteria:
10
Q
RIFLE Category Criteria: I
A
I = Injury
SCr Criteria:
Increase 1-2x OR >50% GFR DECLINE from baseline
Urine Criteria:
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
12
Q
RIFLE Category Criteria: L
A
L = Loss SCr Criteria: Complete loss of Fx Urine Criteria: N/A
13
Q
RIFLE Category Criteria: E
A
E = ESKD SCr Criteria: RRT > 3months (renal replacement therapy) Urine Criteria: N/A
14
Q
AKIN: General Characteristics (3)
A
- ) Defines AKI as “abrupt decrease in kidney Fx” (≤48hr)
- ) NO GFR calculation included in staging
- ) FLE (from RIFLE) included in AKIN Stage 3
15
Q
AKIN: Stage 1
A
SCr Criteria:
SCr ≥ 0.3mg/dL OR 1.5-2x from baseline
Urine Criteria:
16
Q
AKIN: Stage 2
A
SCr Criteria:
2-3x increase from baseline
Urine Criteria:
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:
18
Q
KDIGO: Stage 1
A
SCr Criteria:
Increase ≥0.3mg/dL or 1.5-1.9x from baseline
Urine Criteria:
19
Q
KDIGO: Stage 2
A
SCr Criteria:
Increase 2-2.9x from baseline
Urine Criteria:
0.5mL/kg/hr ≥12hr
20
Q
KDIGO: Stage 3
A
SCr Criteria:
SCr increase 3x from baseline, or SCr ≥4mg/dL, or need of RRT, or eGFR
21
Q
AKI: General Management (7)
A
- ) Hemodynamic Stability
- ) Fluid Management
- ) Electrolyte management
- ) Renal perfusion
- ) Hydration
- ) Eliminate nephrotoxins (if possible)
- ) Renal Replacement Therapy (RRT)
22
Q
KDIGO: AKI Stage 1
A
- ) Non-invasive diagnostic workup
2. ) Consider invasive diagnostic workup
23
Q
KDIGO: AKI Stage 2
A
Stage 1+
- ) Check for drug-dosing changes
- ) Consider RRT
- ) Consider ICU admission
24
Q
KDIGO: AKI Stage 3
A
Stage 1 ,2 +:
Avoid subclavian catheters (if possible)
25
AKI Types + Mortality Rates (3)
Community-acquired AKI (n/a)
Hospital-acquired AKI (15-40%)
ICU-acquired AKI (30-90%)
26
CA-AKI: Risk Factors (5)
1. ) Chronic co-morbid conditions
2. ) Elderly
3. ) Male
4. ) Sepsis/infection
5. ) Drugs (ACEi, arbs, diuretics)
27
HA-AKI: Risk Factors (6)
1. ) Volume depletion
2. ) Hypotension
3. ) Sepsis
4. ) Low cardiac output
5. ) Nephrotoxic drugs
6. ) Radiocontrast dyes
28
ICU-AKI: Risk Factors (6)
1. ) Septic shock
2. ) Major surgery
3. ) Multi-organ failure
4. ) Hypotension
5. ) Low cardiac output
6. ) Nephrotoxic drugs
29
AKI Etiologies (3)
1. ) Pre-renal (glomerulus, arterioles) 70% Cases
2. ) Intrinsic (PCT, LH, DCT, CT(s)) 25% Cases
3. ) Post-renal (bladder, ureter) 5% Cases
30
Post-Renal AKI: Causes (2)
Bladder outlet obstruction
| Ureteral obstruction
31
Post-Renal AKI: Labs + Urinalysis (4)
1. ) BUN : SCr ~ 15
2. ) Urine cellular debris
3. ) Urine : serum osmolality
32
FeNa: Equation
Fractional Excretion of Sodium (limited usefulness with diuretics)
100 x [(Urine sodium x SCr) / ( Urine creatnine x Serum sodium)]
33
Post-Renal AKI: Management
1. ) Obstruction removal
2. ) Alpha-1 blockers (BPH)
3. ) Catheterization
4. ) Percutaneous nephrostomy
34
Pre-Renal AKI: Causes
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
Pre-Renal AKI: Clinical Features
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
Renal Dynamics + ACEi Effects
Prostaglandins/COXs vasodilate AFFERENT
Angiotensin II constricts EFFERENT arteriole
Drop in intraglomerular pressure due to ACE inhibition
37
Pre-Renal AKI: Labs + Urinalysis (4)
1. ) Normal urine sediment (NO CASTS)
2. ) Urine:Serum osmolality > 1.5
3. ) BUN : SCr > 20
4. ) Low FeNa (
38
Pre-Renal AKI: Management (4)
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
Intrinsic AKI
Intra-kidney damage
* vascularture
* glomerulus
* tubules
* interstitium
40
Intrinsic AKI: DI Causes
1. ) Glomerulonephritis (NSAIDs)
2. ) Hemolytic uremic snydrome/TTP (clopidogrel)
3. ) Allergic interstitial nephritis (ABXs)
41
Intrinsic AKI: Tubular Damage
MAJORITY OF CASES (85%)
* 50% --> pre-renal ischemia
* 35% --> direct tubular toxins
42
Intrinsic AKI: Causes + Drugs (6)
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
Post-Ischemic ATN: Pathophys
Prolonged Ischemia resulting in renal damage (parenchyma)
| Severe renal hypoperfusion may result in permanent failure
44
Post-Ischemic ATN: Phases
S/Sx similar to prerenal failure (does NOT resolve with fluid replacement therapy)
1. ) Oliguric/initiation
2. ) Diuretic/maintenance
3. ) Recovery
45
Phases of ATN: Oliguric/Initiation Phase
1-2 Week Duration
* tubular cell death
* diminshed urine output (
46
Phases of ATN: Diuretic/maintenance
* Indicates initial kidney recovery
* increased urine output
* GFR increases gradually
* Na reabsorption/urine concentration increases
47
Phases of ATN: Recovery
* azotemia (5-60d resolution)
* urine concentration within months
* 90-95% GFR return to baseline
* 50% return of baseline (if initial baseline is poor)
48
Post-Ischemic ATN: Labs/urinalysis
1. ) Muddy brown urine
2. ) Granular/epithelial cell casts
3. ) U/S osmolality 2%
6. ) High [Mg++] + tubular enzymes
49
Post-Ischemic ATN: Management
Improve urine output
Restore kidney Fx
Decrease need for RRT
Improved survival
50
AKI: Complications
1. ) Volume overload
2. ) Edema
3. ) Metabolic acidosis
4. ) Malnutrition
5. ) Drug-adjustments
51
Volume Overload: Management
1. ) Fluid restriction
2. ) Diuretics
3. ) Limit Na-intake (DASH diet)
4. ) Dopamine
52
PK: Loop Diuretics
Furosemide (2-2.5hr) RENAL ELIMINATION
***glucouronidated***
Bumetanide (2-2.5hr) HEPATIC ELIMINATION (P450)
Torsemide (6hr) HEPATIC ELIMINATION (P450)
53
Ceiling Dose: Furosemide
IV: 160-200mg (q6h)
PO: >200mg (?)
54
Ceiling Dose: Bumetanide
IV: 8-10mg (q6h)
PO: 8-10mg (QD)
55
Ceiling Dose: Torsemide
IV: 50-100mg (q12h)
PO: 50-100mg (QD)
56
TZD Synergy Doses (2 Rx)
HCTZ (CrCl-based):
> 50mL/min ---> 25-50mg QD
25-50mL/min --> 50-100mg QD
100-200mg/day
Metolazone
5-10mg QD
