Page 92 - Cote clinical veterinary advisor dogs and cats 4th

24 Acute Kidney Injury

• Renomegaly with oliguria/anuria, metabolic acidosis is accident, or fatal arrhythmia due to hyperka-
• Recent-onset polydipsia, polyuria common, and hypocalcemia (e.g., ethylene lemia. Hospitalization of survivors is typically
VetBooks.ir • Multiple animals in same household develop- cholecalciferol-containing rodenticides) is expensive. Animals that recover from AKI may
required for days to weeks, and treatment is
glycol–induced AKI) or hypercalcemia (e.g.,
• Absent urination (no urine production and
no attempts to urinate)
have CKD.
sometimes noted.
ing AKI is consistent with toxin exposure,
especially diet associated • Urinalysis: isosthenuria (consistent finding), Acute General Treatment
tubular casts (common), calcium oxalate
monohydrate crystalluria (associated with Isotonic crystalloid fluid therapy:
PHYSICAL EXAM FINDINGS ethylene glycol toxicity), pyuria (associated • Resolve dehydration within the first 6-12
• Common with pyelonephritis), ± proteinuria, ± hours.
○ Dehydration, halitosis, oral cavity debris/ hematuria, ± bacteriuria ○ Percent dehydration (expressed as a
secretions, ptyalism, normal-sized/enlarged • Abdominal radiographs: renomegaly often decimal [e.g., 10% = 0.1]) × body weight
kidneys present (contrasts with small kidneys often (kg) = deficit (liters)
• May also include identified with CKD) • Compensate for estimated ongoing losses
○ Small bladder • Abdominal ultrasound: renomegaly, renal (e.g., vomiting, panting).
○ Abdominal/renal pain pelvic dilation in association with pyelone- • Provide maintenance fluids (45-60 mL/kg/d).
○ Oral (uremic) mucosal ulcerations phritis, alterations in renal parenchymal ○ Promote diuresis by increasing fluid rate
○ Tachycardia, tachypnea echogenicity often identified, loss of corti- above maintenance once dehydration is
comedullary distinction often identified; resolved. Practically, twice maintenance
Etiology and Pathophysiology hyperechoic cortices (associated with ethylene rates are usually appropriate, assuming
• Renal injury initiated by various causes (e.g., glycol toxicity but also seen in some healthy polyuria has been confirmed and is
ischemia, toxicant, infection) cats) ongoing and overhydration is avoided.
• Renal response causes extension of insult • Electrocardiogram (ECG, p. 1096): altered ○ In oliguric/anuric animals, maintenance
through four mechanisms: by pronounced hyperkalemia (bradycardia fluid rates may be excessive; monitor for
○ Impaired glomerular filtration by reduced [more common in dogs than cats], absent overhydration.
ultrafiltration coefficient P waves, wide QRS complexes) • Avoid overhydration.
○ Tubular obstruction (cellular casts, protein, • Measurement of urine output: assess after ○ Respiratory rate and effort q 1-4h
hemoglobin, crystals) complete rehydration. Although polyuric ○ Body weight q 6-12h
○ Tubular backleak of ultrafiltrate AKI can occur, the classic presentation is ■ Weight loss represents fluid loss or
○ Intrarenal vasoconstriction oliguria or anuria. In contrast, chronic kidney muscle wasting.
• Injury leads to failure of renal excretory, failure is associated with normal or excessive ■ Weight gain in hydrated animal implies
regulatory, and endocrine functions, with volumes of urine. fluid retention (i.e., overhydration).
resultant uremia. ○ Closed-system indwelling urinary catheter
Advanced or Confirmatory Testing facilitates early recognition of polyuria,
DIAGNOSIS • Ethylene glycol testing (positive within 24 oliguria, or anuria in the hydrated animal.
hours of toxin ingestion in dogs, false-positive ○ If oliguria/anuria documented, discontinue
Diagnostic Overview after propylene glycol administration). Cats maintenance fluid therapy, and institute
AKI is suspected when a previously healthy commonly have false-negative ethylene glycol “ins-and-outs” fluid therapy to maintain
animal suddenly develops uremic signs and is test results (p. 314). appropriate hydration.
found to have azotemia and isosthenuria, • Comparison of measured osmolality with ■ Even if anuric, provide 20 mL/kg/d
possibly accompanied by a change in urine calculated osmolality (osmole gap; measured crystalloid fluid (i.e., insensible losses).
output. Often, a risk factor for AKI can be osmolality > 10 mOsm/L above calculated ■ Measure and record urine volume q
identified. A typical approach to diagnosis and osmolality suggests ethylene glycol toxicity) 1-4h. Add that volume of intravenous
treatment is outlined on p. 1398. • Serologic testing or polymerase chain reac- crystalloid to insensible loss for the next
tion: leptospirosis (acute and convalescent 1-4 hours.
Differential Diagnosis titers), Lyme borreliosis, others. Unless ■ Continue until oliguria/anuria resolves.
• Azotemia differential diagnosis another cause of AKI is highly suspected, • Promote urine production with drugs if urine
○ Prerenal azotemia* (dehydration, gastro- all dogs with AKI should be tested for production remains < 1 mL/kg/h despite
intestinal bleeding) leptospirosis (p. 583). appropriate rehydration/fluid therapy.
○ Renal failure (acute or chronic or acute- • Adrenocorticotropic hormone stimulation ○ Furosemide 2-6 mg/kg IV bolus. If oli-
on-chronic failure) test: to rule out hypoadrenocorticism, guria persists, repeat bolus. If urine
○ Postrenal azotemia (urinary tract obstruc- especially with hyperkalemia/hyponatremia production > 1 mL/kg/h after bolus
tion, urinary tract rupture) (p. 512) therapy, institute constant rate infusion
• Renal biopsy: can provide etiologic (0.25-1 mg/kg/h).
Initial Database information ○ Mannitol 250-500 mg/kg IV once.
• CBC: anemia (which often characterizes • Glomerular filtration rate: seldom required Caution: increased vascular volume may
CKD) typically is absent; other changes result in pulmonary edema if overhydrated.
related to cause of AKI (e.g., leptospirosis TREATMENT ○ Dopamine: not recommended
can be associated with neutrophilia and/or • If oliguria or anuria persists despite therapy,
thrombocytopenia) may be identified Treatment Overview institute hemodialysis or peritoneal dialysis,
• Serum biochemical profile: azotemia is a con- Animals with AKI require intensive therapy, or euthanize.
sistent finding (elevated blood urea nitrogen, monitoring, and nursing care. Initial rehy- Address acid-base and electrolyte disorders:
creatinine, phosphorus), hyperkalemia occurs dration and appropriate vascular volume • If potassium > 7 mEq/L: treat hyperkalemia
expansion are imperative. Death is most (p. 495).
often associated with respiratory failure due • If pH < 7.1, institute sodium bicarbonate
*Occasionally, prerenal azotemia and isosthenuria occur simultane- to acute lung injury or pulmonary edema therapy.
ously without kidney disease (e.g., hypoadrenocorticism, aggressive ○ Calculate bicarbonate deficit ([0.3] × [BW
diuretic use, diabetes insipidus). Recognition of these conditions from fluid overload, neurologic compromise
is imperative to avoid overdiagnosis of kidney failure. from uremic encephalopathy or cerebrovascular kg] × [base deficit]).

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