1
Q
Definition of azotemia
A
Elevation in nitrogenous waste products and creatinine
2
Q
Uremia definition
A
Symptoms associated with accumulation of metabolic by-products and endogenous toxins in the blood caused by azotemia
3
Q
Uremia symptoms
A
Fatigue Anorexia N/V Pruritus Mental status changes
4
Q
Normal urine output
A
1 - 1.5L per 24 hours
5
Q
Urine output in non-oliguria
A
> 500 mL/day in patients with renal insufficiency
6
Q
Urine output in oliguria
A
< 400-500 mL/day
7
Q
Urine output in anuria
A
< 50-100 mL/day
8
Q
What is pre-renal AKI?
A
Hypoperfusion of the renal cells
9
Q
What are pre-renal causes of AKI?
A
Intravascular volume depletion
Reduced effective circulating volume
Occlusion of pre-renal vasculature
Drug induced
10
Q
What is intrinsic AKI?
A
Direct damage to the renal cells
11
Q
What are vasculature causes of intrinsic AKI?
A
Thrombotic thrombocytopenia purpura
Hemolytic uremic syndrome
Renal artery thrombosis
12
Q
What are causes of intrinsic AKI due to the glomerulus?
A
SLE
Glomerulonephritis
Post-infection
13
Q
What is AIN?
A
Acute, allergic interstitial nephritis
Inflammatory, immunologic reaction within the renal interstitium
14
Q
What are the causes of AIN?
A
Drugs
Infections
Autoimmune disorders
15
Q
What is ATN?
A
Acute tubular necrosis
16
Q
What are the 3 phases of ATN?
A
Initiation
Maintenance
Recovery
17
Q
What is the initiation of ATN?
A
Damage and decrease in GFR
18
Q
What is the maintenance of ATN?
A
Toxin or ischemia has been removed but the kidney stays in the state
19
Q
What is the recovery of ATN?
A
Building new epithelial
20
Q
What can cause ATN?
A
Extending pre-renal states or exposure to toxins
21
Q
What causes post-renal AKI?
A
Caused by an obstruction in the urinary collection system
22
Q
What are causes bladder outlet obstruction?
A
Prostatic hypertrophy
Cancer
Improperly placed bladder catheter
23
Q
What are causes of ureteral obstruction?
A
Cervical cancers
Retroperitoneal fibrosis
Nephrolithiasis
24
Q
What are causes of renal pelvis/tubules obstruction?
A
Nepholithiasis (crystal deposition from medications)
25
What are RF for AKI?
```
Age (> 65 yo)
Pre-existing renal dysfunction
Volume depletion
Serious infections
Comorbidities
Exposure to nephrotoxins
```
26
What are comorbidities associated with AKI?
HF
CV issues
DM
Liver disease
27
What is AKIN stage 1 SCr criteria?
Increased SCr >/= 0.3
OR
Increased >/= 1.5- to 2-fold from baseline
28
What is AKIN stage 1 UO criteria?
< 0.5 ml/kg/hr x > 6 hours
29
What is AKIN stage 2 SCr criteria?
Increased SCr to > 2- to 3-fold from baseline
30
What is AKIN stage 2 UO criteria?
< 0.5 ml/kg/hr x > 12 hours
31
What is AKIN stage 3 SCr criteria?
Increase SCr to > 3-fold from baseline or SCr >/= 4.0 with an acute increase of at least 0.5
32
What is AKIN stage 3 UO criteria?
< 0.3 ml/kg/hr x 24 hours
OR
Anuria x 12 hours
33
What is KDIGO stage 1 SCr criteria?
1.5-1.9 times baseline
OR
>/= 0.3 increase
34
What is KDIGO stage 1 UO?
< 0.5 ml/kg/h for 6-12 hours
35
What is KDIGO stage 2 SCr criteria?
2.0-2.9 times baseline
36
What is KDIGO stage 2 UO criteria?
< 0.5 ml/kg/h >/= 12 hours
37
What is KDIGO stage 3 SCr criteria?
```
3.0 times baseline
OR
Increase in SCr >/= 4.0
OR
Initiation of renal replacement therapy
OR
In patients < 18 years, decrease in eGFR < 35 ml/min/m2
```
38
What is KDIGO stage 3 UO criteria?
< 0.3 ml/kg/h x >/= 24 hours
OR
Anuria for >/= 12 hours
39
What are the limitations of diagnosis and staging AKI?
Need a baseline SCr level
May be 1-2 day delay to SCr increase after injury
UP can be variable
Primarily studied/validated in critically ill population
40
What are some diagnostic procedures for AKI?
```
Renal ultrasound
Catheter
Kidney-ureter-bladder (KUB) x-ray
Cystoscopy with retrograde pyelography
Renal biopsy
```
41
What are types of Intrinsic AKI?
AIN
| ATN
42
```
How to differentiate causes of AKI: Pre-renal
Physical Exam
Urine Sediment
Urine RBC
Urine Na
FEna
BUN:SCr ratio
```
```
PE: Hypotension, dry mucous membranes, decreased CO, edema, ascites
Urine sediment: Normal
Urine RBC: None
Urine WBC: None
Urine Na: < 20
FEna: < 1
BUN:SCr ratio: >/=20:1
```
43
```
How to differentiate causes of AKI: Intrinsic
Physical Exam
Urine Sediment
Urine RBC
Urine WBC
Urine Na
FEna
BUN:SCr ratio
```
```
PE: Variable
Urine Sediment: GRanular and epithelial casts
Urine RBC: 2-4+
Urine WBC: 2-4+
Urine Na: > 40
FEna: > 2
BUN:SCr ratio: <20:1
```
44
```
How to differentiate causes of AKI: Post-renal
Physical Exam
Urine Sediment
Urine RBC
Urine WBC
Urine Na
FEna
BUN:SCr ratio
```
PE: Prostatic enlargement, bladder distension
Urine sedment: Variable, cellular debris, RBCs, crystals possible
Urine RBC: variable
Urine WBC: 1+
Urine Na: > 40
FEna: Variable
BUN:SCr ratio: 15:1
45
What are non-pharmacologic strategies for prevention of AKI?
Avoidance of nephrotoxins
| Maintain hemodynamic stability to avoid hypotension, hypovolemia
46
What are pharmacologic strategies for prevention of AKI?
Prevention of contrast media-induced nephrotoxicity (CIN)
Sodium bicarbonate + hydration
Loops
47
What is the dose of sodium bicarbonate in AKI?
Alkalinizing agent
Dose - 154 mEq sodium bicarbonate in 1L D5W infuse at 3 mL/kg/h x 1 hr before procedure, then 1 mL/kg/h during procedure and 6 hours after procedure
48
What are the desired goals of AKI treatment?
```
Rapid identification of cause
Removal or reduction of causative agents
Prevent further kidney injury
Prevent complications
Regain renal function
```
49
What is the mainstay of AKI treatment?
Supportive care
50
What is supportive care for AKI treatment?
Stop nephrotoxic drugs
Maintain adequate hemodynamic status
Maintain glucose control
Manage complications
51
What are indications for renal replacement therapy in AKI?
```
A - acid-base abnormalities
E - Electrolyte imbalances (hyperkalemia usually)
I - Intoxications
O - Overload of fluids
U - Uremia
```
52
What are the types of renal replacement therapy?
Intermittent HD (IHD)
Continuous renal replacement therapy (CRRT)
Hybrid
53
What are the causes of diuretic resistance?
```
Excessive sodium intake
Inadequate diuretic dose or inappropriate regimen
Reduce bioavailability
Reduced renal blood flow
Increased sodium reabsorption
```
54
What are the complications of AKI?
```
Fluid overload
Hyperkalemia
Hypernatremia
Infection
CV
GI
Neurologic
```
55
What are the treatments for fluid overload?
Minimize fluid intake
Loop diuretics
Reduction of diuretic resistance
56
What is the most commonly used loop for fluid overload?
Furosemide
57
What is the IV bolus dosing of furosemide in fluid overload?
40-80 mg x 1 (caution - high doses are associated with ototoxicity)
58
Strategies to reduce diuretic resistance
Identify and eliminate/reduce potential cause
Increase dose or use continuous infusion
Add an additional diuretic with a different mechanism
59
Drugs to reduce diuretic resistance
```
Thiazide diuretics (Chlorothiazide 250-500 mg IV q12h)
Thiazide-like diuretics (Metolazone 5-10 mg PO q24h))
```
60
Hyperkalemiain AKI
Most common complication
61
Clinical symptoms of hyperkalemia
Usually asymptomatic
May have palpitations or skipped heartbeats
EKG changes: peaked T waves, prolongation of PR and QRS intervals, disappearance of P wave/merger with QRS and T waves
62
Drugs to treat hyperkalemia
Calcium gluconate (give every pt this)
Insulin (plus glucose)
Albuterol
Sodium polystyrene sulfonate (Kayexalate)
63
Calcium gluconate MOA
Cardioprotection: stabilizes membrane voltage (not a true treatment, does not contribute to K levels at all)
64
Calcium gluconate onset
1-3 minutes
65
Calcium gluconate duration
30 minutes
66
Calcium gluconate comments
May potentiate digoxin toxicity
Give over slow 20-30 minute infusion if patient is on dig
Calcium and bicarb are incompatible
67
Insulin (plus glucose) and Albuterol MOA
Redistribution: increases cellular K uptake to decrease plasma K level
68
Insulin (plus glucose) and Albuterol onset
10-30 min
69
Insulin (plus glucose) Duration
2-6 hours
70
Albuterol duration
2-4 hours
71
Insulin (plus glucose) comments
Glucose given to avoid hypoglycemia
Glucose is unnecessary if BS > 250
Monitor glucose levels closely
72
Albuterol comments
Works better when combined with insulin and glucose
25% of patients do not respond
Tachycardia is common
73
Sodium polystyrene sulfonate MOA
Removal: eliminates K from the gut in exchange for Na
74
Sodium polystyrene sulfonate Onset
1-3 hours
75
Sodium polystyrene sulfonate duration
4-6 hours
76
Sodium polystyrene sulfonate comments
Sorbitol used to minimize constipation
Quicker onset with rectal route
Sorbitol associated with bowel necrosis
May lead to Na retention
77
Hypernatremia treatment
Sodium restriction
78
What is the most common cause of death in AKI?
Infection
79
How can infections cause AKI?
Sepsis can lead to AKI
80
What are CV complications of AKI?
HTN with intermittent hypotension
| CHF, arrhythmias, and pulmonary edema
81
What are the GI complications of AKI?
Increased risk of bleeding
Stress ulceration
N/V
82
What are neurologic complications in AKI?
Altered mental status
Seizures
Somnolence
Renal
flashcards
Decks in class (8)
# Cards
