P. 469

E. Rudloff1
1Lakeshore Veterinary Specialists, Emergency and Critical Care, Glendale, USA
Elke Rudloff, DVM, DACVECC
Lakeshore Veterinary Specialists, Glendale, WI USA
Reduced urine output in the critical patient can represent a functional kidney that is conserving water (e.g. dehydrated patient), reduced renal blood  ow (hypovolemic or hypotensive state), or renal damage. The  rst 2 situations can lead to renal damage, but
are preventable and easily reversed when immediately corrected. Once renal damage has occurred, it is more dif cult to reverse. In dogs, acute kidney injury () has
a mortality rate of up to 60%, with 60% of survivors developing chronic renal failure and 40% having a return to normal function. In cats, the mortality rate is 40-50%, with 50% of survivors developing chronic renal failure.
Acute kidney injury (AKI) is an abrupt decrease in nephron function leading to alterations in the excretory, regulatory, and endocrine function of the kidney resulting in retention of nitrogenous solutes and abnormalities
in acid-base, electrolyte and  uid balance. AKI occurs when >75% of the nephron population is nonfunctioning. Intrinsic AKI results in a reduction in glomerular  ltration rate (GFR) secondary to damage of the renal tubules, interstitium, glomeruli and/or vasculature. Clinically,
is manifest as an abrupt increase in serum creatinine above normal range with a reduced (oliguria or anuria) or increased (polyuria) urine output. Azotemia is an increase in non-protein nitrogenous compounds (e.g. urea and creatinine) in the blood. There can be prerenal, intrinsic renal and post renal causes of azotemia. Uremia is a term used to describe clinical signs and biochemical abnormalities associated with AKI, such as gastroenteritis and hyperparathyroidism.
There are 4 stages to AKI. The initiation phase occurs when a direct insult to the kidneys initiates injury. During the second stage, or the extension phase, ischemia, hypoxia, in ammation and cellular injury continue leading to cellular apoptosis and/or necrosis. The third stage is termed the maintenance phase which is characterized by azotemia and/or uremia, and can last for days to weeks. Oliguria or anuria may occur during this phase. The
fourth stage, or recovery phase is when the renal tubules undergo repair and azotemia improves.
Damage to the glomerulus will result in elevated protein in the urine, many times in absence of azotemia. Persistent glomerular damage will result in altered renal blood  ow and tubular damage/dysfunction. Immune-mediated diseases and amyloidosis are examples. “Lyme nephritis” is a potentially fatal cause of AKI, where immune complexes containing Borrelia antibodies are depositing in the glomerulus. Damage to the tubules will result in isosthenuria and azotemia, and occasionally glucosuria and cellular cylindriuria. Tubular function is normal when urine speci c gravity is highly concentrated or extremely dilute (<1.007).
The rich blood supply makes the kidney highly susceptible to the effects of reduced blood  ow, and blood-borne toxins and infections. Acute tubular necrosis or dysfunction will result when untreated conditions such as hypovolemia, hypotension, systemic in ammatory response syndrome (SIRS), infections, urinary tract obstruction and toxic exposure result in abrupt and sustained reductions in GFR. Reduced GFR results from a combination of vascular (renal vasoconstriction and reduced glomerular ultra ltration coef cient) and tubular (renal tubular obstruction and back-leak of glomerular  ltrate) effects.
A diagnosis of AKI needs to be considered when there is an azotemia and an inappropriate isosthenuria (USG 1.007-1.015). Urine samples are ideally collected
prior to rehydration. Medications such as furosemide may result in isosthenuria, and should be considered when evaluating urine speci c gravity. In addition,
urine dipstick and sediment examination may reveal glucosuria (in the absence of hyperglycemia), proteinuria (in the absence of the presence of in ammatory cells), microscopic hematuria, white and red blood cells, and casts. A laboratory database should also be evaluated for electrolyte abnormalities (particularly potassium, phosphorus, and calcium), venous acid-base disorders, and baseline BUN and creatinine values. The earlier
the intervention, the better the outcome in animals presenting with signs of AKI.
Additional diagnostic testing should include a urine culture, indirect arterial blood pressure, snap 4DX cite test (Borrelia/Anaplasma/Ehrlichia), and leptospirosis serology. If ethylene glycol toxicity is suspected, a diagnosis may be made by using the REACT strips, which can detect ethylene glycol levels as low as 0.6 mg/dL (toxic dose in the cat is 18 mg/dL, dog 50 mg/ dl). Abdominal radiographs may identify calculi involving the urinary tract and abnormal kidney size. Abdominal
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