Acute Kidney Injury

Question 1

What are the different causes of AKI?

Answer 1

1. pre-renal (hemodynamic)
2. renal
3. post renal (obstruction)

Question 2

What are some characteristics of hemodynamic azotemia?

Answer 2

• elevated creatinine and urea
• concentrated urine
• resolves with correction of underlying condition

Question 3

What are some causes of intrinsic renal AKI?

Answer 3

• ischemia
• toxic: ethylene glycol, NSAIDs, cholecalciferol, aminoglycosides (dogs); ethylene glycol, cholecalciferol, lilies (cats)
• infectious ex. Leptospirosis
• primary acute renal disease: immune, neoplastic, degenerative
• systemic disease –> disturbance in hemodynamics ex. FIP, hyperthermia

Question 4

What are the 2 mechanisms of pathophysiology of AKI?

Answer 4

1. intrarenal vasoconstriction
2. tubular dysfunction

Question 5

What are some risk factors of AKI?

Answer 5

1. hospital acquired. Ex. hypovolemia/ hypotension
2. Sepsis. Vasopressor more effective in reducing progression of AKI than norepinephrine (efferent vasoconstriction vs afferent vasoconstriction)
3. Aminoglycosides. Freely filtered and accumulates in renal cortex leading to tubular damage.
4. other antibiotics: expired tetracycline, penicillin, and sulfonamides
   5.NSAIDs

Question 6

Is COX-2 selective NSAIDs safer than none selective ones re: renal toxicity?

Answer 6

No! COX-2 selective is more gentle on the GI system but carries the same risk of nephrotoxicity as non-selective ones

Question 7

What are the treatment principles of AKI?

Answer 7

Rehydration/ fluid therapy

Question 8

Is fluid therapy effective in anuric patients?

Answer 8

fluid therapy should be geared towards replacing insensible losses only (ex. from respiration, 22mL/kg/day)
- if diuresis doesn’t happen or results in over hydration, dialysis will be indicated

Question 9

Which fluid type is associated with lower incidence of AKI?

Answer 9

those with Cl- content approximating plasma –> LRS, plasmalyte vs higher Cl- fluids (ex. 0.9% NaCl) had lower incidence of AKI

Question 10

What’s normal urine volume?

Answer 10

1-2ml/kg/h

Question 11

Do loop diuretics improve outcome in patients with oliguria/ anuria?

Answer 11

no, especially in aminoglycoside toxicity
- should be considered if there is fluid overload or hyperkalemia

Question 12

What’s the role of mannitol in AKI?

Answer 12

has theoretical advantage but not proven in randomized clinical trials

Question 13

What’s the role of calcium channel blockers?

Answer 13

• can reverse renal vasoconstriction
  ex. diltiazem

Question 14

How is hyperkalemia treated?

Answer 14

Acute: calcium gluconate - used to restore cardiac membrane excitability but does not actually lower the K+ level
- insulin will promote intracellular movement of K+ (give dextrose to prevent hypoglycemia)
- sodium bicarbonate can be used, too, to shift the acid/base balance for K+ to go into cells. BUT, the CO2 produced diffuses into CNS and will be converted to H+ –> paradoxical CNS acidosis. SO use with caution if already has increased PCO2 or metabolic alkalosis

Question 15

What drugs can influence extracellular K+ level?

Answer 15

• Albuterol can bind to can move K+
• resin sodium polystyrene sulfonate can bine K+ in the GI tract
• drugs that contributes to hyperkalemia: beta-blockers, digoxin, ACEi, angiotensin receptor blocker, NSAID, k-sparing diuretics, TMS, and total parenteral nutrition

Question 16

How to correct hypokalemia?

Answer 16

oral or IV supplements

Question 17

How to correct hypernatremia?

Answer 17

fluid therapy, can’t go too fast - no more than 12mEq/L per day

Question 18

How to correct metabolic acidosis?

Answer 18

• failing kidneys cant secrete H+ or reabsorb HCO3-
• watch for paradoxical CNS acidosis

Question 19

How to correct hypocalcemia?

Answer 19

• acute decrease in glomerular filtration –> increases phosphorus level –> decreases calcium level (law of mass action)
• stimulates parathyroid
• acidosis increased iCa2+
• tetany
• Ca supplements increases risk of soft tissue mineralization in patients with hyperphosphatemia
• monitor with ECG

Question 20

How to correct hypercalcemia?

Answer 20

• fluid therapy (0.9% NaCl), avoid LRS (contains calcium)
• sodium bicarbonate can also decrease Ca2+ as more bind to protein
• not glucocorticoid responsive
• calcitonin, bisphosphonates (renal toxicity)

Question 21

How to correct increase in Mg?

Answer 21

usually not an issue

Question 22

How to correct phosphorus (PO4) imbalance?

Answer 22

• no specific treatment for decreased PO4 for AKI other than renal replacement therapy
• PO4 binders for food

Question 23

How to correct hypertension?

Answer 23

• need to correct if systolic BP > 180mm Hg
• amlodipine
• avoid ACEi

Question 24

Why is buccal mucosal bleeding time increased in AKI patients?

Answer 24

• uremia can interfere with platelet function

Question 25

What’s the mortality of AKI?

Answer 25

• high
• mild increase in creatinine mortality = 55-58%
• severe hospital acquired AKI - 41-66% dogs, 58-73% cats will die
• community acquired AKI 56% mortality in dogs
• if on hemodialysis: 40-60% will survive
• 20-40% for AKI due to toxin will survive

Question 26

What are other common concurrent disorders with AKI?

Answer 26

• GI upsets
• pancreatitis