An abrupt decline in kidney function is one of the most critical presentations in veterinary emergency and critical care (ECC). Whether triggered by a sudden toxin ingestion, a severe systemic infection, or a period of poor perfusion during shock, acute kidney injury (AKI) represents a metabolic crisis.

Unlike chronic kidney disease (CKD), which is a slow, progressive, and irreversible loss of nephrons, AKI is sudden, highly volatile, and—crucially—has the potential for complete or partial reversibility if caught and managed rapidly.

For the veterinary team, diagnosing and grading AKI requires precise tracking of blood chemistry, electrolytes, and urine output. For the pet owner, AKI is a frightening diagnostic journey: it often involves sudden, severe illness in a previously healthy pet, a high likelihood of intensive care hospitalization, and a complex prognosis that is heavily dependent on the underlying cause.

Understanding the pathophysiology of AKI, the diagnostic criteria of the International Renal Interest Society (IRIS) grading system, cause-specific survival odds, and the treatment pathways—from aggressive fluid resuscitation to advanced hemodialysis—is critical to managing these high-stakes cases.

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Fast Answer: Diagnostics and Treatment Summary

Acute kidney injury (AKI) is a sudden, rapid decline in the kidneys' ability to filter metabolic waste from the blood, resulting in the build-up of toxins (azotemia), electrolyte imbalances, and fluid dysregulation.

It is diagnosed by measuring rising blood creatinine and blood urea nitrogen (BUN) levels, alongside clinical signs of sudden onset: vomiting, anorexia, lethargy, and a marked decrease in urine production.

AKI causes are categorized into:

• Pre-renal: Hypoperfusion due to severe dehydration, shock, heart failure, or heatstroke.
• Intrinsic: Direct structural damage to the kidney tissues, caused by toxins (ethylene glycol/antifreeze, lilies in cats, grapes/raisins in dogs, NSAIDs, aminoglycoside antibiotics) or infections (leptospirosis in dogs, pyelonephritis).
• Post-renal: Obstruction of the urinary tract (ureteral or urethral stones, urethral plugs in cats, or bladder rupture).

Severity is classified using the IRIS AKI Grading System (Grades I through V), which evaluates the degree of blood creatinine elevation and the rate of urine output.

Treatment involves hospitalizing the patient on tailored intravenous (IV) fluids to restore kidney perfusion, administering cause-specific antidotes (such as fomepizole or ethanol for antifreeze poisoning), treating infections with targeted antimicrobials (such as doxycycline for leptospirosis), and managing fluid balance.

If the kidneys shut down and stop producing urine (oliguric or anuric renal failure), or if metabolic waste reaches life-threatening levels despite fluid therapy, hemodialysis (renal replacement therapy) is required to filter the blood while the kidneys attempt to heal.

Prognosis is highly dependent on the cause: dogs with leptospirosis have an 80% to 85% survival rate with prompt care, whereas pets that have already become azotemic from ethylene glycol poisoning carry a grave prognosis, with survival rates below 12% for dogs and 8% for cats.

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AKI vs. CKD: The Critical Distinctions

It is common for pet owners to conflate acute kidney injury with chronic kidney disease. However, these two clinical entities behave in opposite ways, and differentiating them is a critical first step in setting clinical expectations. For the slow, progressive, irreversible form, see our guide to canine chronic kidney disease.

       [ CLINICAL TIMELINE COMPARISON ]
       
Acute Kidney Injury (AKI):
Sudden Insult -> Rapid Decline (Hours/Days) -> [ Resuscitation & Repair ] -> Reversibility Potential
(Pathology: Acute tubular necrosis; tubular basement membrane intact -> cells regenerate).

Chronic Kidney Disease (CKD):
Slow Decline (Months/Years) -> Progressive Nephron Loss -> [ Compensatory Hyperfiltration ] -> Irreversible
(Pathology: Glomerulosclerosis, interstitial fibrosis; lost nephrons replaced by scar tissue).

• Onset: AKI develops over hours to days. CKD develops over months to years, often going unnoticed until 75% of functional nephron capacity is already lost.
• Reversibility: AKI can be reversible. The renal tubular epithelial cells have a high regenerative capacity. If the underlying cause is resolved and the basement membrane of the kidney tubules remains intact, new cells can populate the tubules and restore filtering function over weeks to months. CKD is irreversible; lost nephrons are replaced by fibrous scar tissue, and treatment focuses on slowing progression rather than restoring function.
• Kidney Size: In AKI, the kidneys are typically normal to enlarged, swollen, and painful on abdominal palpation due to acute inflammation and edema. In CKD, the kidneys are typically small, shriveled, irregular, and firm.
• Anemia: Chronic kidney disease is frequently accompanied by a non-regenerative anemia because the damaged kidneys produce less erythropoietin (the hormone that stimulates bone marrow to make red blood cells). AKI patients typically have normal red blood cell counts initially (unless the injury was caused by severe hemorrhage or heatstroke).
• Azotemia Classification: Azotemia (the accumulation of nitrogenous waste in the blood) is classified into three types, which help pinpoint the site of injury:
  1. Pre-Renal Azotemia: The kidneys themselves are healthy, but they are not receiving enough blood flow to filter properly. This is caused by severe dehydration, shock, hypovolemia (blood loss), or decreased cardiac output. It is characterized by high blood creatinine and BUN with concentrated urine (urine specific gravity >1.030 in dogs, >1.035 in cats).
  2. Intrinsic (Renal) Azotemia: The filtration machinery of the kidney (the tubules, glomeruli, or interstitium) is actively damaged. The kidneys cannot concentrate urine, resulting in azotemia with dilute or poorly concentrated urine (isosthenuria, urine specific gravity 1.008–1.012).
  3. Post-Renal Azotemia: The kidneys filter waste successfully, but the waste cannot exit the body due to a downstream blockage (such as a ureteral stone or a blocked urethra) or a rupture in the urinary tract. This causes waste products to back up into the bloodstream.

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Causes of Intrinsic AKI: Toxin and Infection Profiles

Intrinsic AKI is primarily driven by acute tubular necrosis (ATN), where the lining cells of the kidney tubules are destroyed by either ischemic events (lack of oxygenated blood) or direct exposure to nephrotoxins.

1. Nephrotoxins

Ethylene Glycol (Antifreeze)

Ethylene glycol is a sweet-tasting, odorless liquid found in automotive antifreeze, windshield deicers, and heat-transfer fluids. It is extremely toxic: the minimum lethal dose is just 4.4 to 6.6 mL/kg in dogs and a miniscule 1.4 mL/kg in cats (less than a teaspoon for a typical cat).

Ethylene glycol itself is relatively non-toxic to the kidneys; however, it is metabolized by the liver enzyme alcohol dehydrogenase into glycolic acid and oxalic acid. Glycolic acid causes a severe metabolic acidosis.

Oxalic acid then binds with calcium in the bloodstream to form calcium oxalate monohydrate crystals. These needle-like crystals precipitate within the renal tubular lumen, mechanically blocking flow and causing widespread, irreversible necrosis of the tubular cells.

Lilies (Feline Specific)

Cats are uniquely sensitive to plants of the Lilium (e.g., Easter, Tiger, Asiatic lilies) and Hemerocallis (Daylily) genera. All parts of the plant are highly toxic, including the leaves, petals, stems, pollen, and even the water in the vase.

Ingestion of less than a single leaf or licking pollen off the fur causes rapid, severe acute tubular necrosis. The exact toxin has recently been identified as a water-soluble compound that targets the renal mitochondria, destroying the tubular cells' ability to produce ATP.

If untreated, lily ingestion leads to severe, anuric renal failure within 36 to 72 hours.

Grapes and Raisins (Canine Specific)

Grapes, raisins, sultanas, and grape-press cakes can cause unpredictable, idiosyncratic AKI in dogs. While some dogs eat grapes without issue, others develop severe kidney failure after consuming a single grape.

The toxic agent is tartaric acid (and its salt, potassium bitartrate), which is highly concentrated in grapes and tamarinds. Tartaric acid causes acute necrosis of the proximal renal tubules.

Aminoglycoside Antibiotics

Aminoglycosides (gentamicin, amikacin, tobramycin) are highly effective bactericidal antibiotics used for gram-negative infections, but they are classic iatrogenic nephrotoxins.

They are cleared by glomerular filtration and actively accumulated by the proximal renal tubular epithelial cells. Once inside the cells, they disrupt lysosomal membranes, releasing destructive enzymes that cause cell death.

To provide context on how commonly these drugs appear in spontaneous veterinary adverse-event reports, we can examine the FDA's openFDA Animal & Veterinary Adverse Event API — the Center for Veterinary Medicine's spontaneous adverse-event reporting system:

• Gentamicin Sulfate: 1,378 reports (plus Gentamicin: 1,067 reports, totaling 2,445 reports).
• Tobramycin: 179 reports.
• Amikacin: 125 reports.

These reports reflect the ubiquitous clinical presence of these antibiotics, many of which are administered in topical, otic, or ophthalmic formulations, alongside systemic administration where therapeutic drug monitoring is required.

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

NSAIDs (such as carprofen, meloxicam, firocoxib, and robenacoxib) are the backbone of pain management in veterinary medicine. However, they carry a warning for nephrotoxicity, particularly if administered to dehydrated, hypotensive, or pre-existing renal disease patients.

NSAIDs work by inhibiting cyclooxygenase (COX) enzymes, which decreases the production of prostaglandins (specifically PGE2 and PGI2). In healthy, hydrated animals, this has minimal effect on the kidneys.

However, during periods of dehydration, shock, or anesthesia, the kidneys rely on prostaglandins to dilate the afferent arterioles and maintain blood flow to the glomeruli. By blocking prostaglandin synthesis, NSAIDs cause profound renal vasoconstriction, leading to renal papillary necrosis and ischemic AKI.

Note: For detailed statistical profiles on NSAID adverse events, cross-reference our dedicated analysis of veterinary NSAID adverse-event data; we avoid repeating the raw NSAID counts here to keep the focus on the AKI decision.

2. Infectious Causes

Leptospirosis

Leptospirosis is a zoonotic bacterial disease caused by spirochetes of the genus Leptospira. Dogs contract the infection through contact with water, soil, or bedding contaminated with urine from infected wildlife reservoirs (such as rodents, raccoons, or deer).

The spirochetes penetrate mucosal membranes, multiply in the bloodstream, and migrate to the kidneys, where they replicate within the renal tubular lumen. This triggers a severe, acute tubulointerstitial nephritis, leading to AKI.

Because leptospirosis is zoonotic—transmissible to humans through contact with the dog's urine—suspected cases must be isolated immediately with strict PPE protocols. For the infection itself, vaccination, and zoonotic risk, see our guide to leptospirosis in dogs.

Acute Pyelonephritis

This is an ascending bacterial infection of the renal pelvis and parenchyma, typically originating from a lower urinary tract infection (cystitis) that has migrated up the ureters. Escherichia coli is the most common pathogen. It causes severe, localized inflammation, micro-abscess formation, and acute nephron destruction.

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The IRIS AKI Grading System (2026 Revision)

To standardize the diagnosis, severity assessment, and therapeutic tracking of acute kidney injury, the International Renal Interest Society (IRIS) established a grading system. The system evaluates the degree of azotemia and the volume of urine output.

The 2026 IRIS AKI Guidelines grade the severity of injury based on the highest documented blood creatinine concentration compared to the patient's baseline (if known) or the rate of rising creatinine.

IRIS AKI Grade	Blood Creatinine (mg/dL)	Blood Creatinine (µmol/L)	Clinical Characterization	Prognostic Implications
Grade I	< 1.6	< 140	Non-azotemic AKI. Documented rise in creatinine ≥ 0.3 mg/dL within 48 hours, or progressive increase over time.	Excellent to good. Subclinical injury; high potential for full recovery if the insult is halted.
Grade II	1.6 – 2.5	140 – 220	Mild azotemia. Elevated creatinine above normal reference interval with active kidney injury signs.	Good to fair. Low risk of systemic complications, but requires hospitalization for fluid support.
Grade III	2.6 – 5.0	221 – 440	Moderate azotemia. Kidneys are failing to clear waste; electrolyte imbalances (hyperkalemia) are common.	Fair to guarded. Risk of fluid overload; requires intensive monitoring of urine output.
Grade IV	5.1 – 10.0	441 – 880	Severe azotemia. Profound metabolic acidosis; high risk of oliguria/anuria and systemic uremia.	Guarded to poor. Often requires renal replacement therapy (hemodialysis) if medical therapy fails.
Grade V	> 10.0	> 880	Critical, life-threatening azotemia. Severe uremic poisoning, electrolyte disruption, and multi-organ strain.	Grave without dialysis. High mortality; extensive renal tubular damage requires weeks to heal.

Sub-Grading by Urine Output

Alongside the creatinine-based grade, patients are sub-graded by their volume of urine output (UOP) over a 24-hour period, which has a massive impact on fluid management and prognosis:

• Non-Oliguric: UOP > 1.0 mL/kg/hour. The kidneys are still producing a normal volume of urine. This is the safest category for fluid administration.
• Oliguric: UOP between 0.1 and 1.0 mL/kg/hour. Urine production is significantly decreased.
• Anuric: UOP < 0.1 mL/kg/hour (no urine production).

Oliguric and anuric AKI carry a far poorer prognosis. If a dog or cat is receiving IV fluids but cannot produce urine, the excess fluid remains in the blood vessels, raising blood pressure and spilling into the lungs (pulmonary edema) or chest cavity, which can lead to fatal respiratory distress.

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Cause-Stratified Survival Rates: What Decide the Odds?

AKI survival is not a flat statistic. A dog presenting with an IRIS Grade IV AKI due to leptospirosis has a dramatically different prognosis than a dog presenting with the same grade due to antifreeze poisoning.

Underlying Cause	Species Affected	Typical Survival Rate	Primary Prognostic Factors
Leptospirosis	Dogs	80% – 85%	Highly responsive to antibiotics (doxycycline). Prognosis is excellent if started before severe pulmonary hemorrhage develops.
Lily Ingestion	Cats	80% – 95% (if treated early) / < 10% (if delayed)	If aggressive IV fluid therapy is started within 18 hours of ingestion, survival is near 100%. Once anuria develops (36-48 hours post-ingestion), survival is extremely low without hemodialysis.
Grape / Raisin Toxicity	Dogs	50% – 55%	Highly unpredictable. Approximately 50% of exposed dogs develop severe AKI; of those that become azotemic, the survival rate with supportive care is roughly 53%.
Ethylene Glycol (Azotemic)	Dogs & Cats	12% (Dogs) / 8% (Cats)	Grave once the patient is already azotemic. The calcium oxalate crystals have permanently destroyed the tubular basement membranes. Survival is near 100% only if the antidote is given within 8 hours of ingestion.
Ureteral Obstruction	Cats	85% – 90%	Highly survivable if the blockage is bypassed. Placement of a Subcutaneous Ureteral Bypass (SUB) device has a success rate of 90%.
Pyelonephritis	Dogs & Cats	55% – 60%	Dependent on antibiotic resistance. Prognosis is good if the bacteria are sensitive to fluoroquinolones or penicillins.
Overall Clinic Cohorts	Dogs & Cats	40% – 50%	A broad retrospective cohort of dogs and cats hospitalized with AKI shows an overall case fatality rate of 34% (early diagnostics) to 60% (emergency referral centers).

Note: Data compiled from retrospective studies in the Journal of Veterinary Emergency and Critical Care (JVECC), JAVMA, and tertiary referral centers.

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The Treatment Protocol and the Management Ladder

Managing a patient with acute kidney injury is a balancing act. The veterinary clinician must follow a structured management ladder, adjusting the protocol hourly based on blood pressure, electrolyte levels, and urine production.

       [ THE AKI CLINICAL TREATMENT LADDER ]
       
Level 4: Renal Replacement Therapy (Hemodialysis)
  - Indicated for refractory oliguria/anuria, severe hyperkalemia, or fluid overload.
  ^
Level 3: Diuretic Challenge & Electrolyte Correction
  - Fenoldopam, Furosemide, or Mannitol to convert oliguria to polyuria. Insulin/Dextrose for Hyperkalemia.
  ^
Level 2: Target Therapy & Antidotes
  - Fomepizole/Ethanol for Antifreeze (within 8h). Doxycycline for Leptospirosis. SUB device for obstruction.
  ^
Level 1: Perfusion Restoration & Fluid Resuscitation
  - Tailored IV fluids (Isotonic crystalloids) matching hydration deficits and ongoing losses.

Level 1: Fluid Resuscitation and Perfusion

The primary goal in early AKI is to restore blood flow to the kidneys. Ischemic nephrons cannot heal without oxygenated blood.

• Resuscitation: If the animal is in shock, IV fluid boluses are administered.
• Rehydration: The patient's dehydration deficit is calculated (e.g., % dehydration × body weight in kg = liters of fluid needed) and replaced over 12 to 24 hours.
• The Input-Output Rule: To prevent the fatal complication of fluid overload, the veterinary team must measure ins and outs. The patient is fitted with an indwelling urinary catheter connected to a closed collection system. The volume of IV fluids administered is matched to the volume of urine produced, plus calculated "insensible losses" (fluid lost through panting and saliva).

Level 2: Target Therapy and Antidotes

If a specific cause is identified early, targeted interventions are deployed:

• Antifreeze Poisoning: Fomepizole (4-methylpyrazole or 4-MP) is a competitive inhibitor of alcohol dehydrogenase. If administered within 8 hours of ingestion in dogs, it prevents the formation of the toxic calcium oxalate crystals, allowing the ethylene glycol to be excreted safely in the urine.
  • Note on Cats: Cats require a much higher dose of fomepizole than dogs, and it must be administered within 3 hours of ingestion to be effective. If fomepizole is unavailable, medical-grade Ethanol (alcohol) can be administered IV; the liver will prioritize metabolizing the ethanol, leaving the ethylene glycol to pass out in the urine.
• Leptospirosis: Suspected dogs are immediately started on Ampicillin IV (to clear the active blood infection) followed by Doxycycline (oral or IV, to clear the bacteria from the renal tubules).
• Ureteral Obstruction: If an ultrasound confirms a stone blocking a ureter, a surgeon must relieve the pressure. In cats, this is routinely performed by placing a Subcutaneous Ureteral Bypass (SUB) device, which connects the kidney pelvis directly to the urinary bladder, bypassing the blocked ureter. For the more common urethral blockage in male cats — a separate post-renal AKI cause — see our guide to urinary obstruction in cats.

Level 3: Diuretic Challenge and Electrolyte Correction

If the kidneys are not producing urine despite hydration being restored (oliguric/anuric state), the clinician will attempt to restart the kidneys' pumps:

• Diuretic Challenge: Medications like furosemide or mannitol are administered to force the tubules to dump fluid, trying to convert an oliguric AKI into a polyuric (high-urine-output) state. If the kidneys do not respond to a diuretic challenge, fluid rates must be dialed down to a minimum maintenance level to avoid pulmonary edema.
• Hyperkalemia Management: As the kidneys fail to excrete potassium, blood potassium rises (hyperkalemia). High potassium disrupts the electrical conduction of the heart, leading to bradycardia (slow heart rate), arrhythmias, and eventual cardiac arrest. Emergency treatments include:
  • Calcium Gluconate IV: Protects the heart muscle cells from the toxic effects of potassium (does not lower potassium levels).
  • Dextrose and Regular Insulin IV: Insulin drives potassium out of the blood and back inside cells; dextrose is given concurrently to prevent hypoglycemia (low blood sugar).

Level 4: Hemodialysis (Renal Replacement Therapy)

When the kidneys are completely shut down (anuric) or when medical therapy can no longer control the uremic toxins, hyperkalemia, or fluid overload, the patient has reached the top of the management ladder.

Hemodialysis is the only therapy that can save their life.

• How it works: The patient is fitted with a specialized, large-bore double-lumen catheter in their jugular vein. The blood is pumped out of the body, passed through an external dialyzer membrane (which filters out creatinine, urea, potassium, and excess water), and returned to the body.
• Indications for Dialysis:
  • Oliguria or anuria that fails to respond to fluid therapy and diuretics.
  • Severe hyperkalemia (>6.5–7.0 mEq/L) that does not respond to medical therapy.
  • Severe fluid overload (weight gain, pulmonary edema, pleural effusion).
  • Ingestion of dialyzable toxins (ethylene glycol, if treated within the first 24 hours).
• Availability and Cost: Hemodialysis is highly specialized. It is only available at major veterinary university teaching hospitals or select specialty emergency referral centers. A typical course of dialysis involves hospitalization for 1 to 3 weeks, requiring multiple runs (usually every other day). The cost is substantial, frequently ranging from $10,000 to $20,000, which represents a significant financial barrier for many pet owners.
• Clinical Outcomes: A landmark study by Eatroff et al. (JAVMA 2012) evaluated the outcomes of 135 dogs and cats with AKI treated with intermittent hemodialysis. The study reported that 53% of dogs and 50% of cats survived to discharge. While this statistic may seem modest, it represents patients that were otherwise 100% fatal under standard medical management. Of the survivors, approximately half recovered normal kidney function, while the other half transitioned into manageable chronic kidney disease.

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FAQs: Acute Kidney Injury in Pets

Is acute kidney injury in dogs reversible?

Yes, acute kidney injury can be fully or partially reversible. Unlike chronic kidney disease, where nephrons are permanently lost, the cells lining the kidney tubules can regenerate after an acute insult. If the dog is supported with IV fluids or hemodialysis to keep them stable and keep their electrolyte levels safe, the kidney cells can multiply and repopulate the tubules over a period of 2 to 4 weeks, restoring kidney function.

How long can a dog or cat live after acute kidney injury?

If a pet survives the initial acute phase (typically the first 7 to 14 days of hospitalization) and their kidney function returns to baseline, their life expectancy can be completely normal. However, if the kidneys suffer severe structural damage, the pet may recover only partial function, leaving them with residual chronic kidney disease. These patients will require lifelong management (special diets, hydration support); for cats, our feline CKD treatment guide walks through that long-term plan. With good management they can still live for months or years.

What is the survival rate for ethylene glycol (antifreeze) toxicity?

The survival rate is near 100% only if the dog or cat receives the antidote (fomepizole or ethanol) within 3 to 8 hours of ingestion. Once a pet has become azotemic (showing high creatinine and BUN on blood work, typically 12 to 24 hours after ingestion), the survival rate drops precipitously to less than 12% for dogs and 8% for cats under standard medical care, as the calcium oxalate crystals have already destroyed the kidney architecture.

Do all cats with lily exposure get kidney failure?

Yes. Cats are uniquely sensitive to lilies, and ingestion of even a tiny amount of pollen, a single leaf, or drinking water from a vase containing lilies will cause severe, acute tubular necrosis in virtually 100% of exposed cats. If a cat is brought to a veterinary clinic and started on aggressive IV fluid therapy within 18 hours of exposure, the kidneys can be protected and survival is near 100%. If treatment is delayed beyond 24 to 36 hours, severe kidney failure is almost guaranteed.

How much does hemodialysis for a pet cost, and where is it available?

Hemodialysis for dogs and cats is a highly specialized therapy available only at major veterinary university hospitals or select urban specialty referral centers. The cost is high, typically requiring an initial setup and catheter placement fee, followed by a per-treatment charge. A typical course of treatment for acute kidney injury involves 1 to 3 weeks of hospitalization and costs between $10,000 and $20,000.

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Sources

• International Renal Interest Society (IRIS): IRIS AKI Grading Criteria (2026 Revision). URL: https://www.iris-kidney.com/iris-guidelines-1
• Today's Veterinary Practice: A Guide to Acute Kidney Injury in Small Animals. URL: https://todaysveterinarypractice.com/internal-medicine/a-guide-to-acute-kidney-injury-in-small-animals
• Journal of the American Veterinary Medical Association (JAVMA): Long-term outcome of cats and dogs with acute kidney injury treated with intermittent hemodialysis: 135 cases (1997–2010). URL: https://avmajournals.avma.org/view/journals/javma/241/11/javma.241.11.1471
• PubMed Central (PMC): Acute kidney injury in dogs: Etiology, clinicopathologic findings, prognostic markers, and outcome. URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC8965273
• Veterinary Ireland Journal: Management of acute kidney injury in the dog and cat. URL: https://www.veterinaryirelandjournal.com/images/pdf/small/sa_dec_2017.pdf
• U.S. Food and Drug Administration (FDA): openFDA Animal & Veterinary Adverse Event API (Center for Veterinary Medicine adverse-event reporting system). URL: https://api.fda.gov/animalandveterinary/event.json