Acute kidney injury (AKI) is defined as an abrupt reduction in kidney function resulting in alterations in glomerular filtration, urine production, and tubular function.
Overview and Clinical Importance
Acute kidney injury (AKI) is defined as an abrupt reduction in kidney function resulting in alterations in glomerular filtration, urine production, and tubular function. AKI represents a continuum from mild nephron injury to severe, life-threatening kidney failure. The term AKI has largely replaced "acute renal failure" in veterinary medicine, allowing for greater stratification of severity and earlier treatment intervention.
Feline AKI is a commonly encountered emergency in small animal practice. Cats present unique challenges due to their small ureteral diameter (approximately 0.4 mm), making them highly susceptible to obstructive uropathy, and their sensitivity to certain nephrotoxins such as lilies and ethylene glycol.
| Stage |
Description and Clinical Features |
| 1. Initiation |
Duration: Hours to days. Original insult occurs (ischemia, toxins, infection, obstruction). GFR begins to fall but clinical signs often absent. Therapeutic window exists for early intervention. |
| 2. Extension |
Duration: 1-2 days. Ongoing hypoxia and inflammatory response. Tubular cells undergo necrosis and apoptosis. GFR continues to decline. Early laboratory changes may become apparent. |
| 3. Maintenance |
Duration: Days to weeks. Characterized by azotemia and uremia. Oliguria (less than 0.5 mL/kg/h) or anuria may occur. Tubular repair begins. Maximum supportive care required. |
| 4. Recovery |
Azotemia improves. Renal tubules undergo repair and regeneration. Marked polyuria may occur (post-obstructive diuresis). Recovery may be complete or result in residual CKD. |
Pathophysiology of AKI
AKI results from direct damage to renal tubular cells and ischemia, leading to inability to maintain fluid, electrolyte, and acid-base balance. The pathophysiology can be described in four distinct stages:
High-YieldThe initiation and extension phases represent the critical therapeutic window. Once the maintenance phase is established, treatment focuses on supportive care while awaiting tubular regeneration.
| Category |
Causes |
Key Features |
| Pre-renal |
Hypovolemia, hypotension, shock, cardiac failure, anesthesia-induced hypotension |
Volume responsive. USG greater than 1.035-1.040. Resolves with fluid therapy. |
| Intrinsic Renal |
Nephrotoxins (lilies, ethylene glycol, NSAIDs, aminoglycosides), pyelonephritis, leptospirosis, renal lymphoma, ischemia |
Isosthenuria (USG 1.008-1.015). Not volume responsive. Requires supportive care. |
| Post-renal |
Ureteral obstruction (calcium oxalate stones), urethral obstruction, uroabdomen |
Requires imaging. Ureteral obstruction common in cats. Surgical/interventional treatment often needed. |
Etiologies of Feline AKI
AKI causes are classified as pre-renal, intrinsic renal, or post-renal:
Lily Toxicity (Lilium and Hemerocallis species)
Clinical Significance: True lilies (Lilium spp.) and day lilies (Hemerocallis spp.) are UNIQUELY toxic to cats and represent one of the most common causes of nephrotoxic AKI in feline practice. As little as 2 leaves or part of a single flower can cause fatal nephrotoxicosis. ALL parts of the plant are toxic, including pollen, leaves, petals, and even vase water.
Timeline of Clinical Signs:
- 1-3 hours: Vomiting, hypersalivation, anorexia, depression
- 12-30 hours: Polyuria/polydipsia, progressive dehydration
- 24-48 hours: Oliguria progressing to anuria, severe azotemia
- 48-72 hours: Death if untreated
Treatment Protocol:
- Decontamination: Induce emesis if within 2 hours, activated charcoal with cathartic
- IV Fluid Diuresis: Lactated Ringer's solution at twice maintenance (130 mL/kg/day) for minimum 48-72 hours
- Monitoring: Serial renal values every 12-24 hours, urine output monitoring
- Hemodialysis: Consider early hemodialysis for toxin removal; required for anuric patients (survival approximately 18% with dialysis)
NAVLE TipOn NAVLE, remember: Cat + vomiting + lily exposure = IMMEDIATE aggressive IV fluid therapy. Treatment must begin within 18 hours for best prognosis. Cats treated early with decontamination and fluid diuresis have survival rates approaching 100%. Once anuria develops, prognosis is grave without hemodialysis.
Ethylene Glycol Toxicity
Clinical Significance: Ethylene glycol (EG) from antifreeze is highly toxic to cats, with a lethal dose of less than 1.5 mL/kg. Cats are twice as sensitive as dogs. The sweet taste makes it palatable, and even minimal exposure can be fatal.
Triphasic Clinical Presentation:
Diagnostic Findings:
- Calcium oxalate monohydrate crystalluria (highly suggestive in cats)
- Severe metabolic acidosis with increased anion gap
- Hypocalcemia (calcium binds to oxalate)
- Ultrasound: Hyperechoic renal cortex ("bright kidneys"), loss of corticomedullary distinction
Treatment - CRITICAL TIME WINDOW:
Antidote (Fomepizole): Must be administered within 3 HOURS of ingestion in cats!
High-YieldCATS REQUIRE 6X THE DOSE OF FOMEPIZOLE compared to dogs because feline alcohol dehydrogenase is less effectively inhibited. Treatment beyond 3 hours post-ingestion has mortality rates approaching 97-100%.
Ureteral Obstruction
Clinical Significance: Ureteral obstruction is increasingly recognized as a cause of feline AKI. The feline ureter has an internal diameter of only 0.4 mm, making it highly susceptible to obstruction. Greater than 90% of feline ureteroliths are calcium oxalate and cannot be dissolved medically.
Clinical Presentation:
- Vague signs: lethargy, anorexia, vomiting, weight loss
- Abdominal pain, especially on renal palpation
- Asymmetric kidney size (enlarged obstructed kidney)
- Small bladder (anuria) or normal bladder (unilateral obstruction)
- Many cats have pre-existing CKD with acute decompensation
Diagnostic Imaging Findings:
- Radiography: May show radiopaque ureteroliths, but many are small and difficult to visualize
- Ultrasound: Pyelectasia (pelvic dilation greater than 3 mm suggestive), hydroureter, nephromegaly, retroperitoneal fluid
- Antegrade pyelography/CT: May be needed to confirm obstruction location
Treatment Options:
NAVLE TipSUB placement is the current gold standard for feline ureteral obstruction per ACVIM consensus. Creatinine at presentation correlates with survival: cats with creatinine less than 440 umol/L (IRIS AKI 1-3) have median survival of 949 days vs 530 days for those with higher creatinine (IRIS AKI 4-5).
| Phase |
Clinical Signs |
| Phase 1 (0-12 hrs) |
CNS depression, "drunk" appearance, ataxia, vomiting, PU/PD, hypothermia, seizures. Appears to transiently improve. |
| Phase 2 (12-24 hrs) |
Cardiopulmonary: Tachycardia, tachypnea, severe metabolic acidosis, dehydration, depression worsens. |
| Phase 3 (24+ hrs) |
Oliguric/anuric renal failure, severe azotemia, hyperkalemia, death within 72 hours if untreated. |
IRIS AKI Grading System
The International Renal Interest Society (IRIS) has developed a grading system for AKI to facilitate classification, prognostication, and treatment decisions. Unlike CKD staging, AKI grading reflects a dynamic, unstable condition.
Sub-grading: Each grade is further classified based on: (1) Volume responsive or non-responsive, (2) Oliguria/anuria present or absent, (3) Requirement for renal replacement therapy
| Treatment |
Feline Dosing |
| Fomepizole (4-MP) |
125 mg/kg IV initially, then 31.25 mg/kg IV at 12, 24, and 36 hours (6x higher dose than dogs!) |
| Ethanol (alternative) |
5 mL of 20% ethanol/kg IV initially, then every 6 hours for 5 treatments, then every 8 hours for 4 treatments |
Diagnostic Approach
Differentiating AKI from CKD
High-YieldMany cats with AKI have underlying CKD (acute-on-chronic). Look for signs of both! A cat with small irregular kidneys AND acute worsening of azotemia likely has AKI superimposed on CKD.
Ultrasonographic Findings in Feline AKI
Common ultrasound findings in cats with AKI (in order of frequency):
- Nephromegaly (70%): Kidney length greater than 4.5 cm. Most common finding in AKI.
- Pyelectasia (60%): Pelvic dilation greater than 3 mm. Severe pyelectasia (greater than 10 mm) highly suggestive of obstruction.
- Increased medullary echogenicity (51%): Indicates tubular damage or crystalline deposition.
- Increased cortical echogenicity (40%): Hyperechoic cortex. In ethylene glycol toxicity, appears "brighter than spleen."
- Retroperitoneal fluid (33%): Associated with oliguria/anuria - POOR PROGNOSTIC INDICATOR.
| Treatment |
Description |
Outcomes |
| Medical Management |
IV fluids, diuretics, smooth muscle relaxants (prazosin, tamsulosin) |
Only 8-13% resolution rate. Surgery if no improvement in 24-48 hours. |
| SUB Device |
Subcutaneous ureteral bypass - nephrostomy catheter connected to cystostomy catheter via subcutaneous port |
Preferred treatment. MST greater than 2 years. Requires q3-6 month flushing. 48% major complication rate (manageable). |
| Ureteral Stent |
Double pigtail stent placed within ureteral lumen |
Technically challenging in cats. Higher complication rates than SUB including dysuria (17-35%), re-obstruction (22%). |
Treatment of Feline AKI
Fluid Therapy - The Cornerstone of Treatment
Goals: Restore hydration, correct electrolyte/acid-base abnormalities, optimize renal perfusion, promote diuresis.
Exam Focus: Normal urine output is greater than 1-2 mL/kg/hour. Oliguria is defined as less than 0.5 mL/kg/hour. An indwelling urinary catheter is essential for monitoring AKI patients.
Diuretic Therapy for Oliguria/Anuria
Important: Diuretics increase urine output but do NOT improve GFR or proven to improve outcomes. They facilitate fluid management and may indicate less severe injury if patient responds.
Management of Hyperkalemia
Life-threatening complication. ECG changes: Tall peaked T waves, shortened QT, wide QRS, small/absent P waves, bradycardia, sine wave, ventricular fibrillation.
| Grade |
Creatinine |
Clinical Description |
Urine Output |
| Grade I |
Less than 1.6 mg/dL (less than 140 umol/L) |
Non-azotemic AKI. Evidence of AKI (biomarkers, glucosuria, casts). Volume responsive. |
Usually normal or polyuric |
| Grade II |
1.7-2.5 mg/dL (141-220 umol/L) |
Mild AKI with mild azotemia. Stable or progressive increase in creatinine. |
Variable |
| Grade III |
2.6-5.0 mg/dL (221-439 umol/L) |
Moderate AKI. Increasing azotemia. Clinical signs becoming apparent. |
May be oliguric or polyuric |
| Grade IV |
5.1-10.0 mg/dL (440-880 umol/L) |
Severe AKI. Uremic signs present. May require RRT. |
Often oliguric/anuric |
| Grade V |
Greater than 10.0 mg/dL (greater than 880 umol/L) |
Life-threatening AKI. Severe uremia. Dialysis typically required. |
Typically anuric |
Prognosis
Prognosis depends heavily on etiology, severity, and rapidity of treatment:
High-YieldOliguria/anuria indicates GRAVE prognosis regardless of etiology unless dialysis is available. Response to diuretics suggests less severe injury. Cats may recover completely or have residual CKD requiring lifelong management.
| Parameter |
AKI |
CKD |
| History |
Acute onset, often known exposure or event |
Chronic PU/PD, weight loss over weeks to months |
| Body Condition |
Usually normal or mildly decreased |
Often poor (BCS less than 2/9), muscle wasting |
| Kidney Size |
Normal or enlarged, smooth contour, may be painful |
Small, irregular, non-painful |
| PCV |
Usually normal (non-regenerative anemia uncommon) |
Non-regenerative anemia common |
| Potassium |
Often hyperkalemia (especially oliguric/anuric) |
Often hypokalemia |
| Ultrasound |
Nephromegaly, pyelectasia, retroperitoneal fluid, hyperechoic cortex |
Small kidneys, irregular contour, loss of corticomedullary definition |
| Phase |
Protocol |
| Initial Rehydration |
Calculate deficit: % dehydration x body weight (kg) x 1000 = mL. Replace over 2-6 hours. Use balanced crystalloid (LRS preferred). |
| Maintenance + Ongoing |
Insensible losses: 22 mL/kg/day. Match "Ins and Outs" - replace urine output + insensible losses q4-6h. |
| Oliguric/Anuric Patient |
CAUTION: Do NOT continue aggressive fluids if no urine production! Risk of fluid overload. Consider diuretics or dialysis. |
| Drug |
Dose |
Notes |
| Furosemide |
Initial: 1-2 mg/kg IV bolus. If no response, double q1h (up to 6 mg/kg). CRI: 0.25-1 mg/kg/hr |
First-line diuretic. CRI more effective than bolus in dogs. Response indicates less severe injury. |
| Mannitol |
0.25-0.5 g/kg IV over 15-20 min. May repeat q4-6h or CRI 1-2 mg/kg/min |
CONTRAINDICATED if overhydrated or anuric. Risk of volume overload and osmotic nephrosis. Not recommended by some authors. |
| Treatment |
Dose |
Mechanism/Notes |
| Calcium gluconate 10% |
0.5-1.5 mL/kg IV slow over 5-10 min with ECG monitoring |
Cardioprotective. Does NOT lower K+. Immediate but transient (20-30 min). |
| Regular Insulin + Dextrose |
Insulin 0.5 U/kg IV + Dextrose 1-2 g per unit insulin given |
Shifts K+ intracellularly. Onset 15-30 min. Monitor glucose q1-2h. |
| Sodium Bicarbonate |
1-2 mEq/kg IV slow |
Corrects acidosis, promotes kaliuresis. Use if concurrent metabolic acidosis. |
| Etiology |
Prognosis |
Key Factors |
| Lily toxicity (early) |
EXCELLENT if treated within 18h. Survival approaching 100% |
Treatment delay critical. Anuria = poor prognosis |
| Lily toxicity (late/anuric) |
POOR. Approximately 18% survival with hemodialysis |
Dialysis only option once anuric |
| Ethylene glycol (within 3h) |
GOOD if fomepizole given within 3 hours |
3-hour window CRITICAL in cats |
| Ethylene glycol (late) |
GRAVE. Mortality 97%+ if treatment delayed beyond 3h |
Antidote ineffective once renal damage occurs |
| Ureteral obstruction (SUB) |
FAIR to GOOD. MST greater than 2 years. Creatinine-dependent |
Creatinine less than 440 umol/L = better prognosis |
| Ischemic AKI |
REASONABLE if patient can be supported 1-2 weeks |
Tubular regeneration possible |