Acute Kidney Injury

Question 1

define acute kidney injury

Answer 1

sudden onset renal parenchyma injury ranging from subclinical/subcellular to fulminant excretory failure (wide spectrum of disease)

mostly based on increases in creatinine

Question 2

acute renal failure

Answer 2

• advanced/overt subset of AKI
• failure to meet excretory, metabolic, and endocrine demands
• leads to retention of uremic toxins and fluid, electrolyte, and acid-base disorders

Question 3

acute kidney disease

Answer 3

kidney damage following AKI lasting > 7 days but < 90 days

Question 4

T/F: non-azotemic AKI is a thing

Answer 4

T, increases by a small/non-azotemic amount can still have significant changes in mortality

Question 5

what are pre-renal and post-renal etiologies of AKI?

Answer 5

pre-renal: decreased renal blood flow volume and increased renal vasoconstriction

post-renal: urinary tract obstruction and urinary tract rupture

Question 6

what are some intrinsic/renal etiologies?

Answer 6

Ischemia: shock, anesthesia, renal thrombosis

primary renal dz: pyelonephritis, leptospirosis, acute glomerulonephritis, lymphoma

systemic disease: SIRS, sepsis, pancreatitis, malignant hypertension

nephrotoxins: ethylene glycol, grapes/raisins, lillies, cholecalciferol, NSAIDs, aminoglycosides

Question 7

in the RAAS system where do NSAIDs have an effect?

Answer 7

Prostaglandin PG2E resulting in vasoconstriction of the afferent renal ateriole -> decreased renal blood flow and GFR

Question 8

In the RAAS system where do ACEi’s have an effect?

Answer 8

Angiotensin II resulting in dilation of the efferent renal arteriole (by reducing angiotensin II synthesis/effects) -> decreased glomerular hydrostatic pressure and GFR

Question 9

clinical presentation of dog with AKI

Answer 9

acute onset non-specific lethargy and GI Signs

• increased/decreased urine
• dehydrated
• oral ulceration
• melena
• tongue tip necrosis
• scleral injection
• bradycardia
• peripheral edema

Question 10

Lab findings for AKI

Answer 10

CBC: hemoconcentration or anemia

Chemistry:
- azotemia
- hypo or hyperkalemia
- hyperphosphatemia
metabolic acidosis

Question 11

dx approaches for AKI

Answer 11

• abdominal rads and AUS
• FNA and biopsy
• ethylene glycol test
• Lepto PCR
• serology/pcr for RMSF, Ehrlichia, lyme, babesia, leishmania

Question 12

4 phases of fluid therapy

Answer 12

ROSE

1. resuscitation: isotonic crystalloid IV bolus
2. optimization: rehydration, maintenance, ongoing losses
3. stabilization: insensible losses + urine output +/- ongoing losses
4. evacuation: gradual decrease in fluids

Question 13

LRS, PLyte-148 Normosol-R

Answer 13

balances, polyionic, buffered, isotonic
- all good choices for resuscitation and replacement

Question 14

0.9% NaCl

Answer 14

• not the fluid of choice for most AKI cases
  -no buffer, excess Na and Cl

Question 15

0.45% NaCl + 2.5% dextrose,
50% LRS + 2.5% dextrose

Answer 15

ideal fluids for maintenance due to lower Na+ load

Question 16

what are clinical signs of fluid overload?

Answer 16

peripheral edema, increases RR, increased weight >10% from non-dehydrated baseline, serous ocular and nasal discharge, chemosis, cavitary effusions

Question 17

main consequences of fluid overload

Answer 17

decreased GFR and worsening azotemia

Question 18

causes of oligo-anuria

Answer 18

• decreased renal perfusion
• altered glomerular permeability
• backflow of glomerular filtrate
• tubular obstruction from casts or cell debris

tx with diuretics, renal vasodilators, etc.

Question 19

indications for renal replacement therapy

Answer 19

• progressive azotemia or severe refractory signs
• severe hyperkalemia or acid-base disturbances not responsive to medical therapy
• oliguria or anuria
• life threatening fluid overload
• acute intoxication with substances that can be removed by dialysis

Question 20

prognosis of AKI

Answer 20

mortality rates approximately 50%, infectious is better than ischemic or toxic