Acute Kidney Disease Management
World Small Animal Veterinary Association Congress Proceedings, 2017
Elke Rudloff, DVM, DACVECC
Lakeshore Veterinary Specialists, Emergency and Critical Care, 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 flow (hypovolemic or hypotensive state), or renal damage. The first 2 situations can lead to renal damage, but are preventable and easily reversed when immediately corrected. Once renal damage has occurred, it is more difficult 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 fluid balance. AKI occurs when >75% of the nephron population is nonfunctioning. Intrinsic AKI results in a reduction in glomerular filtration 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 postrenal 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, inflammation 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 flow 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 specific gravity is highly concentrated or extremely dilute (<1.007).

The rich blood supply makes the kidney highly susceptible to the effects of reduced blood flow, and blood-borne toxins and infections. Acute tubular necrosis or dysfunction will result when untreated conditions such as hypovolemia, hypotension, systemic inflammatory response syndrome (SIRS), infect ions, 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 ultrafiltration coefficient) and tubular (renal tubular obstruction and back-leak of glomerular filtrate) 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 specific gravity. In addition, urine dipstick and sediment examination may reveal glucosuria (in the absence of hyperglycemia), proteinuria (in the absence of inflammatory 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 ultrasound is useful for detecting pyelectasia, calculi, mass lesions, and other intraabdominal abnormalities that may be related to azotemia. Occasionally a ureteral obstruction may require contrast pyelography to diagnose.

A classification scheme has been proposed for staging V in dogs (Table 1; Thoen 2011).

Table 1. Proposed veterinary acute kidney injury (V) staging system for dogs

V Stage


Stage 0

Creatinine increase <150% from baseline

Stage 1

Creatinine increase of 150–199% from baseline
Creatinine increase of 26.5 mmol/L (0.3 mg/dl) from baseline

Stage 2

Creatinine increase of 200–299% from baseline

Stage 3

Creatinine increase of ≥300% from baseline
An absolute creatinine value >354 mmol/L (4.0 mg/dl)


All critically ill animals are at risk for sustaining AKI. Maintaining hydration and renal perfusion will reduce risk of renal toxicity, and all critically ill patients should have renal parameters monitored daily (Creatinine, UO, electrolytes).When potentially nephrotoxic agents are used in the critical dog, daily comparison of urine GGT to creatinine ratio to baseline values may uncover early renal toxicity.


Circulatory abnormalities (hypotension, poor perfusion, arrhythmias) caused by hypovolemia and hyperkalemia must be rapidly corrected. The mainstay to treatment of AKI is to reperfuse the kidneys and promote excretion of toxic substances. Because AKI and hypovolemia generally cause an acidosis, a balanced buffered isotonic crystalloid is chosen for resuscitation and rehydration.

Small volume resuscitation techniques to normal perfusion endpoints are used until urine output is better characterized. Once perfusion has been restored, tissue hydration deficits are calculated and replaced over 4–10 hours. The calculated volume to replace is based on hydration status and laboratory parameters.

% dehydration x body weight (kg) = L of fluid required for replacement

In addition to the volume being administered for rehydration, sensible and insensible losses need to be accounted for (1–2 ml/kg/h). Finally, ongoing losses from vomiting, diarrhea, respiratory disease, polyuria, etc., need to be calculated and replaced. These fluids are estimated, or can be measured. Urine output can be monitored by a variety of ways: 1) a urinary catheter can be placed and attached to a closed collection system; 2) the urine can be collected during walks; 3) the urine can be quantified using a metabolic cage; 4) the bedding can be weighed (1 g=1 ml urine); and 5) weighing the animal. Fluid balance can be complicated in the AKI patient. Determination of fluid rates is best determined by closely monitoring and comparing fluid losses with infusion volumes, and monitoring central venous pressure.

Pharmacological intervention may be necessary when uremia is present, infection is suspected or hypertension is present. H2-blockers reduce acid secretion and reflux as well as promote mucosal healing when gastritis or uremic ulcers are suspected. Pantoprazole (0.7 mg/kg IV q 24h) is the preferred drug by the authors during hospitalization. Liquid sucralfate (0.5–1 g PO q6–8h) may coat an area of uremic erosion once vomiting is controlled. When vomiting from stimulation of the chemoreceptor trigger zone in the brain is suspected, substance-P and serotonin inhibitors, such as maropitant (2–8 mg/kg PO; 1 mg/kg SQ q 24h), and ondansetron (0.1–0.3 mg/kg SQ TID, or 0.5 mg IV load then 0.5 mg/kg/h CRI) or dolasetron (0.5 mg/kg IV, SQ q 24h), may also be helpful. Placement of a nasogastric tube can aid in decompressing the stomach and reducing nausea, as well as provide a means for administering medications and nutritional support. Early feeding using liquid diets can imp rove gastrointestinal function and recovery rate. When it is periodically suctioned, the volume can be used in calculation for ongoing fluid losses.

Phosphate binders (aluminum hydroxide, aluminum carbonate, calcium acetate) may decrease phosphate absorption when the patient has hyperphosphatemia. Acid-base disorders generally correct with adequate fluid resuscitation and reestablishing urine output.

For cases suspected to have a urinary tract infection, broad-spectrum antibiotics covering for many aerobic infections are administered intravenously. Ampicillin (22 mg/kg IV q6h), ampicillin-sulbactam (22 mg/kg IV q6h), and cefazolin (22 mg/kg IV q 8h) are good choices. It is preferred that a urine sample for culture is obtained prior to starting antibiotics.

In the cardiovascularly stable patient, diltiazem (0.3–0.5 mg/kg slow push [10 min] followed by 3–5 µg/kg/min constant rate infusion [CRI] x 48 to 96 hours) can also lower the creatinine more effectively than diuresis alone in dogs with leptospirosis. A lowering of ∼15 mm Hg systolic blood pressure is expected, and heart rate and blood pressure must be frequently monitored.

Hypertension is not unexpected once fluid replacement has been achieved. If the systolic blood pressure exceeds 150 mm Hg or diastolic blood pressure exceeds 90 mm Hg, an antihypertensive agent should be considered. A calcium channel blocker (diltiazem as listed above), oral hydralazine (0.5–2 mg/kg PO q12h) or amlodipine (0.2–0.4 mg/kg PO q12h in dogs, ¼ of a 2.5-mg tablet PO once daily in cats) can be administered. Hydralazine usually has an effect within hours of administration, while amlodipine may not decrease blood pressure for 24 hours after administration.

Diuretics such as furosemide will not improve outcome, but are occasionally given to increase urine volume when overhydration is a complication in the face of oliguria (<0.27–1 ml/kg/h). Furosemide, 2 mg/kg bolus infusion is followed by a continuous rate infusion of 1 mg/kg/h. Diuretics can result in dehydration and hypovolemia if urine output is not monitored and fluid balance adjusted.

Renal replacement therapy is a final method which can rapidly eliminate toxic byproducts in the plasma. Indications for dialysis include severe, intractable uremia, severe hyperkalemia, intractable volume overload, and acute toxicities.


References are available on request.


Speaker Information
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Elke Rudloff, DVM, DACVECC
Lakeshore Veterinary Specialists
Glendale, WI, USA

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