Acute Renal Failure Flashcards

1
Q

What is acute renal injury?

A

Encompasses mild damage that does not cause azotemia to severe damage associated with anuria

May be pre-, post-, or renal

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2
Q

Is acute renal injury reversible or irreversible?

A

Reversible

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3
Q

What is acute renal failure?

A

Decreased GFR leading to retention of nitrogenous wastes

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4
Q

What is the RIFLE criteria?

A

Allows the clinician to objectively and uniformly define AKI

R: Risk
I: Injury
F: Failure
L: Loss
E: End stage kidney disease
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5
Q

What is the RIFLE criteria based on?

A

Proportion of serum creatinine increases and urine output decreases

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6
Q

What is the issue with using the RIFLE criteria in vet med?

A

Good baseline references for creatinine may not have been established at presentation

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7
Q

What is the IRIS AKI subgrading based on?

A

Same thing as RIFLE, creatinine to urine output

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8
Q

What is pre renal AKI due to?

A

Anything that causes insufficient blood flow to the kidney

Hypoxia, ischemia, dehydration, hypovolemia, hypotension, decreased circulatory volume, anesthesia, hypoadrenocorticism, trauma, sx, shock, heatstrocke, hypoalbuminemia, hypoperfusion (NSAID tox)

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9
Q

What is pre-renal AKI characterised by?

A

Reduced fractional excretion of sodium

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10
Q

What are some renal etiologies for AKI?

A
  • Prolonged hypoperfusion
  • Prolonged obstruction
  • Excessive vasoconstriction
  • Thrombosis/DIC
  • Transfusion reaction
  • Infection
  • Immune diseases
  • Neoplasia
  • Secondary to systemic disease
  • Nephrotoxins
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11
Q

What are some post-renal etiologies for AKI?

A

Urine leakage or obstruction causing damage to collecting tubules

May result in urine leakage and uroabdomen

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12
Q

What are the four phases of acute renal failure?

A

Initial, extension, maintenance, and recovery

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13
Q

What are the characteristics of the initial phase of AKF?

A
  • Usually little to no clinical signs

- Decrease in urine output or increase in creatinine

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14
Q

Is intervention necessary in the initial phase of ARF?

A

Yes

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15
Q

What are the characteristics of the extension phase of ARF?

A

Continued hypoxia and inflammation

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16
Q

What part of the nephron is particularly susceptible to toxins and ischemia?

A

Proximal tubule and loop of henle

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17
Q

What is the maintenance phase of ARF?

A

Lasts 1-3 weeks typically, urine is usually ultrafiltrate and may be decreased or increased volume

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18
Q

What is the recovery phase of ARF?

A

Characterized by polyuria and extreme los of sodium

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19
Q

How long may the recovery phase of ARF last?

A

Weeks to months depending on damage

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20
Q

What causes intra-renal vasoconstriction?

A

Imbalance between the vasoconstrictors (endothelin) and vasodilators (NO)

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21
Q

What is the consequence of intra-renal vasoconstriction?

A

Endothelial injury, decreased oxygen, ATP deficiency, mitochondrial damage, oxidant injury, intracellular acidosis and hypercalcemia

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22
Q

What are the causes of tubular dysfunction?

A
  • Tubular obstruction from crystals or detached RTE cells
  • Cytoskeletal injury with loss of polarity
  • Loss of tight junctions between cells
  • Cell necrosis
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23
Q

What are some risk factors for ARF?

A

Dehydration, hypovolemia, anesthesia, hypoxia, SIRS

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24
Q

How do you prevent ARF?

A

Aggressive treatment of shock and dehydration, avoid nephrotoxic drugs especially in compromised patients

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25
What needs to be monitored closely in acute renal patients?
Dehydration status, blood volume and pressure, cardiac and urine output, GFR (direct if necessary)
26
What are some renoprotective drugs?
- Calcium channel blockers (prevent Ca influx) - Selective DA-2 receptor agonists (vasodilation) - Selective DA-1 receptor agonists (prevents vasoconstriction) - Erythropoeitin analogues (protect against hypoxia)
27
Should fluids be given to accute renal patients?
Yes, always, helps correct electrolyte abnormalities as well as pressure and volume issues
28
Why should ECG be monitored in acute kidney patients?
To asses patient for electrolyte associated arrhythmias
29
Can pressors be given to acute renal patients?
Yes, if hypotension cannot be resolved with fluid therapy
30
How do you diagnose acute renal issues?
- Correction of underlying cause - Detection of reduced urine output - Urinalysis - Azotemia - Reduced fractional excretion of sodium - Renal tubular biomarkers
31
What are the initial bolus doeses to correct shock in the dog and the cat?
Dog: 60-90 mL/kg Feline: 45 mL/kg Over 60 min in 15 min interval boluses
32
What is the formula to correct dehydration?
%dehydration x 10 x BK kg = mL to be given over 6-12 hours
33
What volume accounts for insensible fluid loss?
22 mL/kg/day
34
What volume accounts for sensible fluid loss?
44 mL/kg/day
35
What is the maintenance fluid rate?
60 mL/kg/Day but adjust for abnormal urinary losses
36
What should be used for rehydration of the ARF patient?
Crystalloids or hypertonic saline
37
What are the four fluid requirements?
1. Dehydration 2. Insensible losses 3. Ongoing losses 4. Sensible losses
38
What is oliguria defined as?
39
Is oliguria always a bad thing?
No, normal in a dehydrated patient
40
How do you treat pathological oliguria?
Mannitol, furosemide, dopamine, Ca channel blockers
41
Is treatment of oliguria usually successful?
No, no evidence that treatment improves outcome
42
What is mannitol?
An osmostic diuretic used to decrease cell swelling | Has some free radical scavenging ability
43
What are some contraindications for mannitol use?
Dehydration or anuria
44
What is furosemide?
Loop diuretic that inhibits Na-K-2Cl symporter in thick ascending loop of henle
45
What is the advantage of fruosemide?
Decreases O2 requirement of the kidney and increases urine production without increase in GFR, renoprotective and fast acting
46
What are some contraindications of furosemide?
Dehydration, lethargy, tachycardia, ototoxicity
47
Is dopamine an effective treatment for oliguria in cats?
No
48
When is dopamine beneficial as a pressor?
When ARF is secondary to cardiac output failure or severe hypotension
49
What does fenoldopan do?
Increase urine output
50
What is the MOA of calcium channel blocker in oliguric patients?
Pre-glomerular vasodilation by preventing Ca from moving intracellularly
51
When are calcium channel blockers usually used in kidney patients?
Post-transplant as a renoprotective agent or in standard care of lepto patients
52
What are definitive treatments for acute renal failure?
Extracorporal renal replacement therapy (dialysis), peritoneal dialysis
53
What is dialysis?
Use of artificial membranes with created hydrostatic and solute concentrations designed to mimic kidney function
54
What are some indications for ERRT/dialysis?
- Fluid overload with pulmonary edema - Hyperkalemia - Progressive azotemia - Acute toxicity
55
Is peritoneal dialysis a simple useful procedure?
No, only used in ICU situations and has short survival times
56
What is the most common complication of peritoneal dialysis?
Acute uremia
57
What are some other complications of peritoneal dialysis?
Dialysis disequilibrium syndrome and blockage of the drain
58
What is the specific therapy for ethylene glycol toxicity?
4-methylpyrazole within 8 hours of ingestion Ethanol can work as well
59
What is the specific therapy for NSAID toxicity?
Misoprostal
60
What is the specific therapy for lepto patients?
Penicillins and doxycycline
61
What is the specific therapy for pyelonephritis patients?
Culture/Sensitivity, fluoroquinolones or TMS for 4-6wks
62
What is the specific therapy for aminoglycoside toxicity?
Ticarcillin IV (binding agent)
63
What is the specific therapy for TMS toxicity?
Urinary alkalinization
64
Why do acute kidney patients develop hyperkalemia?
Inability to excrete potassium due to damage to pumps
65
What can result from hyperkalemia?
Acidosis, bradycardia, sinus arrest, muscle weakness, ileus
66
How is hyperkalemia treated?
Insulin and dextrose infusion Calcium gluconate Correction of metabolic acidosis
67
Why do acute kidney patients develop acidosis?
Failure to absorb bicarb or excrete hydogen
68
How do you correct acidosis?
IV bicarb
69
T/F: Hypocalcemia is a common complication of acute kidney patients.
False- rare complication
70
What is hypocalcemia associated with in kidney patients?
Deficiency of calcitriol
71
How is hypercalcemia corrected?
Diuresis or ERRT, calcitonin, biophosphates
72
Is there a specific therapy for hyperphosphatemia?
No, reduce phosphorus intake or use binders in food
73
Why do kidney patients develop hypertension?
RAAS activation and fluid overload
74
What drugs should be avoided in ARF patients?
Ace inhibitors
75
Which drugs should be considered to correct hypertension in acute kidney patients?
Amlodipine and hydralazine
76
What are some aspects of GI supportive care in the acute renal patient?
Control of anorexia, nausea, and vomiting | Contorl uremic gastopathy
77
What are some strategies for dietary supplementation in renal patients?
Enteral feeding device, renal prescription diet
78
What acute kidney conditions have a good outcome usually?
Dialysis, leptospirosis, obstructive and infectice issues
79
What acute kidney conditions have a poor outcome usually?
No ECRR when indicated, decreased urine production, hypothermia, hyperkalemia, toxins (especially ethylene glycol)