Acute Kidney Injury: Causes, Diagnosis, and Treatment Flashcards
compare and contrast azotemia and uremia
azotemia: biochemical abnormality, defined as elevation or buildup of nitrogenous products (BUN, creatinine, SDMA) in the blood
uremia: constellation of clinical signs associated with the accumulation of substances (uremic toxins) usually excreted in the urine under normal physiologic conditions
uremic animals ARE azotemic, but azotemic animals might not be uremic
-BOTH can occur in AKI or CKD
describe intrinsic renal causes of AKI
damage to any section of the kidney: glomeruli, tubules, interstitium, or vessels
- ischemic: renal vascualr disease (thrombosis, DIC, stenosis) or due to any of the hemodynamic factors
- nephrotoxicants
-ethylene glycol
-aminoglycosides
-NSAIDs
-lilies (cats)
-grapes/raisins (dogs)
-and many more!!!
most commonly intrinsic AKI follow ischemic or toxic tubular damage!!
- immune-mediated/inflammatory:
-immune-mediated glomerulonephritis, systemic lupus erythematosus - infectious: -pylonephritis (escending infection or hematogenous), enterobacteriacea
-lepto - neoplasia: lymphoma
- prolonged (several days) urinary obstruction
-not a blocked cat, will die first
describe ethylene glycol
source: automotive antifreeze (seasonal in many places), heat exchange fluid, some photographic fluid
species affected: various; common in cats and dogs
pathophysiology of AKI
-toxic metabolites cause
-severe metabolic acidosis
-calcium oxalate monohydrate (CaOx) and hippuric acid precipitate in renal tubules and result in tubular epithelial necrosis secondary to CaOx in tubular lumen
describe phases of ethylene glycol toxicosis
- within 1 hour of ingestion animal is ataxic/drunk +/- GI signs, then becomes asymptomatic
- 12-24hrs after: cardiopulmonary involvement can occur (inconsistently)
- 1-3 days later: oliguric AKI (BAD), renomegaly, and signs of acute renal failure
describe treatment of ethylene glycol AKI
- early recognition: induction of emesis, ideally within the hour
- antidote treatment:
-4-methylpyrazole (4MP or fomepizole) or ethanol
-inhibit conversion to to toxic metabolites and allow more to be excreted in urine
-ideally within 8 hours in dogs and 3 hours in cats - hemodialysis can remove absorbed EG from blood
- supportive: IV fluid to promote renal blood flow
prognosis: once renal damage has occur, prognosis is poor
describe diagnosis of ethylene glycol AKI
- often too late :(
- early labs:
-hypocalcemia and high anion gap metabolic acidosis - ethylene glycol testing:
-serum lab test and cage side tests - imaging:
-enlarged, hyperechoic kidneys +/- echogenic rim at the corticomedullary junction
describe aminoglycosides
source: bactericidal time dependent antibiotics, prescribed by us!
species: any
pathphysiology of AKI:
1. accumulate in proximal renal tubular cells and cause lysosomal rupture/mitochondrial injury, resulting in tubular cell death
- nephrotoxic potential: neomycin > gentamicin > tobramycin > amikacin > streptomycin
- dose and duration dependent risk: avoid prolonged course
- risk increases with:
-preexisting renal disease
-fever, sepsis, dehydration, or electrolyte disturbances
-concurrent furosemide theraphy
describe diagnosis, treatment, and prognosis of aminoglycoside toxicity
diagnosis:
1. monitor urinalysis daily to ID cylinduria or isosthenuria
2. urinary cystatin B is a newer option
3. monitor BUN/creatinine every 1-2 days
treatment:
1. stop the drugs
2. supportive care
prognosis:
usually reversible if detected early and drug discontinued
describe NAIDs nephrotoxicity
source: us/owner
species:
any! toxicity is species and formulation dependent
pathophysiology:
1. interfere with renal autoregulation
2. inhibition of cyclooxygenases decreases prostaglandins and causes afferent arteriolar constriction
3. higher risk if other factors present (volume depletion, concurrent use of diuretics, or vasoactive drugs)
describe diagnosis, treatment, and prognosis of NSAID nephrotoxicity
diagnosis:
1. known exposure
2. animals present with GI signs, GI bleeding, abdominal pain, AKI
3. ensure baseline labwork with urinalysis
treatment:
1. early recognition: GI decontamination, activated charcoal and/or cholestyramine resin (bile acid sequestrant)
- supportive: IV fluids
- GI protectants/antacids
- IV lipid emulsion: make lipid sink
- extracorporeal therapies: total plasma exchange or plasmapharesis
prognosis: depends
describe nephrotoxicity from lillies
source: household, all members of genera lilium and hemerocallis are nephrotoxic to cats
-any part of the plant is toxic (flower is hella toxic)
species: cats and meerkat
pathophysiology:
1. specific toxin unknown
-diffuse tubular necrosis, particularly proximal tubule: evidence of AKI within 24-72 hours, often progress to oliguria/anuria and death
-transient gastritis
describe diagnosis, treatment, and prognosis of lily toxicity
diagnosis:
1. known exposure
2. vomiting, PU/PD
3. neuro signs rare but can occur
4. azotemia, glucosuria, proteinuria, isosthenuria
treatment:
1. early gastric decontamination (emesis) and activated charcoal
2. bathe the cat to avoid ingestion during grooming
3. supportive: IV fluids or hemodialysis
prognosis:
1. treated early can do well
2. often fatal for cats presented in the maintenance phase of AKI
describe grapes/raisins/currants
source: owners and environment
species: dog (most severely) and also cats (less severely)
pathophysiology of AKI
1. toxic compound thought to be tartaric acid and its salt potassium bitartrate
-acute renal tubular necrosis (esp proximal tubule)
-azotemia within 2 days of ingestion
-ologuria or anuria in 50% of cases
2. varying toxic doses!
other signs:
1. vomiting, diarrhea, abdominal pain
describe diagnosis, treatment, and prognosis of grape/raisin/currant tox
diagnosis:
1. known exposure
2. azotemia, hypercalcemiua, hyperphosphatemia, and other evidence of AKI
treatment:
1. early gastric decontamination
2. supportive
prognosis:
-50% survival; survivors can return to normal kidney function
describe clinical presentation of AKI
- history:
-asymptomatic: found on labwork or
-hx of recent anesthesia, access to outdoors, vx for lepto, meds in house, environment, plants, treats - anorexia
- lethargy
- nausea or vomiting
- diarrhea
- weakness
- PU/PD and/or oliguria/anuria
+/- acute CNS signs (early EG)
+/-history of risk factors
usually <1 week in duration!
