Contributors: Melissa Wallace, Rosanne Jepson

 Species: Canine   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading


  • Acute kidney injury: the term acute kidney injury or AKI is now the preferred terminology when referring to acute damage occurring to renal parenchyma or rapid decline in renal function. It is recognized that acute kidney injury represents a spectrum of disease ranging from acute changes in renal function that may be clinically imperceptible through to complete failure of the kidneys to meet excretory, metabolic and endocrine demands. This stage may appropriately be termed acute renal failure (ARF) and renal replacement therapy may be considered. Further information regarding the recently released International Renal Interest Society AKI grading scheme can be found
  • Cause: pre-renal, intrinsic renal (toxins/drugs, infection, ischemia, vascular), post-renal (obstruction).
  • Signs: dependent on severity of renal injury. At mildest clinical signs may not be apparent but AKI may be detected on the basis of biochemical, urinalysis, diagnostic imaging findings compatible with AKI. At most severe, typically short duration (<1 week) with clinical signs including lethargy, weakness, vomiting, diarrhea, anorexia, dehydration, neurological signs. Patients may present with oliguria (in most cases), anuria or polyuria (less commonly).
  • Treatment: prompt therapy to maintain renal perfusion, remove toxin/drug exposure, limit renal damage, resolve any post-renal obstruction, provide on-going support for kidney.
  • Prognosis: prognosis is dependent on extent of initial renal insult. Extensive renal damage will result in death (unless renal replacement therapy is provided). With less extensive renal insult prognosis for patient will depend on treatment of underlying cause of AKI and recovery of renal function. Full spectrum is possible from apparent recovery of renal function (subsequently categorized as IRIS stage I CKD due to prior known renal insult) through to IRIS stage IV CKD.

Presenting Signs

  • Dependent on severity of AKI:
    • At mildest may have no apparent presenting signs and yet AKI can be demonstrated on the basis of biochemical, urinalysis and diagnostic imaging findings (Table 1).
  • Acute uremia Uremia (nausea, vomiting, hypersalivation, diarrhea, anorexia, lethargy, weakness).
  • Oliguria (absolute oliguria well hydrated patient <0.5-1 ml/kg/h).
  • Oral ulceration appears in //www.vetlexicon.com3-5 days with uremic halitosis.
  • Anuria.
  • Polyuria (>2 ml/kg/h) in recovery phase.
  • Abdominal pain in sublumbar region/palpation of kidneys (depending on etiology).
  • Uremic encephalopathy (seizures) in very advanced cases.
  • Neurological signs may also be appreciated with ethylene glycol toxicity Ethylene glycol poisoning.
  • Uremic pneumonitis (respiratory distress) in very advanced cases
  • Clinical signs compatible with post-renal obstruction, eg stranguria, dysuria.

Acute Presentation

  • Anuria or oliguria.
  • Uremic crisis: severe lethargy, weakness, anorexia, vomiting, halitosis, oral ulceration.

Geographic Incidence

  • Infectious disease may have geographical influence, eg Leptospirosis Leptospirosis , Borrelia burgdorferi Borreliosis.
  • Access to certain toxins may have geographic influence, eg Ethylene glycol toxicity.

Cost Considerations

  • Intensive care and monitoring required is expensive with guarded prognosis. Renal replacement therapy (eg intermittent hemodialysis/continuous renal replacement therapy) comes with additional expense and commitment and prognosis remains guarded in many cases.

Special Risks

  • Volume overload: excess fluid administration with inadequate urine output. Significant morbidity factor.
  • Hyperkalemia Hyperkalemia : can result in atrial standstill, complete heart block and cardiac arrest.
  • Severe metabolic acidosis Acid base imbalance (pH <7.1) can cause cardiac problems and exacerbate neurological signs.
  • Consider dose and frequency of any drugs requiring renal excretion. Potential for overdose/delayed excretion.
  • Barrier nursing if concern re zoonotic disease, eg Leptospirosis.




Renal ischemia



Predisposing Factors

  • Any cause of reduced renal blood flow.


  • Hypoperfusion: hypovolemia, decreased cardiac output, systemic hypotension, increased blood viscosity.
  • Anesthesia/surgery, especially without appropriate blood pressure monitoring and IV fluid support.
  • Administration/accidental misuse of known nephrotoxic medications, eg NSAIDs.
  • Access to known nephrotoxins, eg ethylene glycol/grapes or raisins.
  • Exposure to infectious agents, eg Leptospirosis.
  • Pre-existing disease, eg cardiac disease, chronic kidney disease Kidney: chronic kidney disease (CKD).
  • Sepsis Shock: septic , systemic inflammatory response syndrome, multi-organ dysfunction Multiple organ dysfunction syndrome (MODS).


  • Pre-renal: insufficient delivery of blood to functional kidneys to allow adequate clearance of solutes and waste products.
  • Intrinsic renal: damage to any section of the kidney, eg glomerulus, tubular cell, interstitium or vessels. Most is the result of acute tubular damage due to ischemic or toxic injury. Prolonged pre-renal hypoperfusion may lead to intrinsic kidney damage. Prolonged post-renal obstruction may also lead to intrinsic renal injury.
  • Post-renal: urine leakage or obstruction at post-renal site, eg urethral obstruction Urethra: obstruction , bilateral ureteral obstruction or unilateral obstruction with single functioning kidney.
  • Four phases of AKI:Initiation phase(inciting injury),extension phase(continued hypoxia and inflammatory response extends renal damage),maintenance phase(period of 1-3 weeks during which a critical degree of damage has occurred),recovery phase(increased urine output with variable sodium loss, regeneration of impaired tissue and nephrons may take weeks to months).
  • Nephrons are damaged at different sites (glomerulus, tubular cell, intercellular junction, basement membrane) depending on etiology → acute decline in glomerular filtration rate due to intrarenal vasoconstriction and/or tubule dysfunction → hypoxia particularly affecting the medulla and mitochondrial damage → decreased availability of ATP leads to energy deficit → reduced activity of active transport pumps, eg Na+ K+ ATPase → disruption to concentration gradients → cell swelling, tubular obstruction and vascular congestion → cytoskeletal damage, impaired tubular cell polarity and redistribution of Na+ K+ ATPase pumps from apical to basolateral membrane, loss of tight junction function → cell sloughing and tubular obstruction (cell necrosis and aggregation with cast formation).
  • Renal recovery → survival of sub-lethally injured tubular cells, which regain polarity and function.


  • Animals may die acutely, especially if underlying etiology unknown, specific treatment not available and oliguria/anuria persists resulting in severe metabolic derrangements (eg hyperkalemia and metabolic acidosis).
  • If treated appropriately, animals may recover, but recovery phase can take >3 weeks of intensive care with ultimate outcome being long-term chronic kidney disease


Presenting Problems

  • Vomiting.
  • Anorexia.
  • Lethargy.
  • Weakness.

Client History

  • Usually < 1 week duration implying acute nature of disease.
  • Lethargy.
  • Anorexia.
  • Vomiting.
  • Diarrhea/melena.
  • Oliguria (less common, anuria or polyuria).
  • Exposure to drugs/toxins.
  • Anuria.
  • Polyuria.
  • Neurological signs.
  • Halitosis.
  • Post-renal AKI: patients may exhibit additional clinical signs if urethral obstruction present.

Clinical Signs

  • Enlarged kidneys.
  • Oral ulceration, halitosis.
  • Pyrexia in pyelonephritis.
  • Dehydration.
  • Hypovolemia.
  • Bradycardia.
  • Hypothermia.
  • Melena.
  • Abdominal pain (sublumbar/renal).
  • Systemic hypertension Hypertension.

Diagnostic Investigation


Table 1: International Renal Interest Society Acute Kidney Injury Grading Scheme (2013) (Adapted

AKI gradeBlood creatinineClinical description
*Substaging: Each grade of AKI is further subgraded as
1. Non-oliguric (NO) or oligoanuric (O)
2. Requiring renal replacement therapy (RRT
I*<1.6 mg/dL
<140 µmol/l
Non Azotemic AKI:

a) Documented AKI: Historical, clinical, laboratory
(eg glucosuria, cylinduria, proteinuria, inflammatory sediment, microalbuminuria)
or imaging evidence of AKI, clinical oliguria/anuria, volume responsiveness
b) Progressive non-azotemic increase in blood creatinine;
>=0.3mg/dL/ >=26.4 µmol/l within 48 hours
c) Measured oliguria (< 1ml/kg/hr) or anuria over 6 hours
II*1.75-2.5 mg/dL
141-220 µmol/l
Mild AKI:

a) Documented AKI and static or progressive azotemia
b) Progressive azotemic increase in blood creatinine;
>=0.3mg/dL/ >=26.4 µmol/l within 48 hours or volume responsiveness
c) Measured oliguria (< 1ml/kg/hr) or anuria over 6 hours
III*2.6-5.0 mg/dL
221-439 µmol/l
Moderate to severe AKI:

a) Documented AKI and increasing severities of azotemia and functional renal failure
IV*5.1-10.0 mg/dL
440-880 µmol/l
V*>10.0 mg/dL
>880 µmol/l

Complete blood count Hematology: complete blood count (CBC)

  • May be unremarkable.
  • Anemia may be present (gastrointestinal blood loss/volume overload/red cell fragility).


  • Plain abdominal radiography Radiography: abdomen :
    • Assessment of renal size, shape, mineralisation, for evidence of urolithiasis Urolithiasis (nephrolith/uterolith/urethrolith).
  • Kidneys may be enlarged in acute inflammatory conditions.
  • Contrast radiography:

2-D Ultrasonography
  • Kidney ultrasonography Ultrasonography: kidney.
  • Enlarged kidneys (compare with normal Kidney normal long-axis - ultrasound Kidney: normal short-axis - ultrasound ).
  • Assessment of renal shape, size and architecture:
    • Bright (hyperechoic) renal cortex in ethylene glycol cases.
    • Often enlarged kidneys with AKI.
    • Pyelectasia - consider with pyelonephritis, recent fluid therapy, obstructive disease dependent on severity.
    • Hydronephrosis Hydronephrosis / hydroureter (consider secondary to obstructive disease).
    • Peri-renal fluid accumulation.
    • Loss of corticomedullary differentiation.
  • Assessment for post-renal obstruction (nephrolith/ureterolith/urolithiasis).
  • Evidence of concurrent disease affecting other organs.

Infectious disease testing

  • See ECG overview ECG: overview.
  • Changes are usually due to hyperkalemia:
    • Flattened or absent P waves, progressing to heart block, atrial standstill.
    • Increased PR interval.
    • Increased QRS interval.
    • Bradycardia.

  • Renal aspirate: may be performed with ultrasound guidance:
    • Definitive diagnosis may be made for conditions such as renal lymphosarcoma Kidney: neoplasia.
    • Limited by lack of architectural detail.
  • Biopsy Biopsy: kidney :
    • Ultrasound guided trucut biopsy (common), surgical biopsy (uncommon).
    • Renal histopathology may help in identification of underlying aetiology of AKI.
    • Provides information on extent of renal damage and evidence of renal recovery.
    • Caution with uncontrolled systemic hypertension, bleeding diatheses, thrombocytopenia, administration of antithrombotic therapy, eg aspirin Acetyl salicylic acid.

Gross Autopsy Findings

  • Identify primary cause:
    • Pre-renal: hypovolemia or cardiac shock (prerenal).
    • Intrinsic renal disease.
    • Post-renal: obstruction, bladder rupture and uroperitoneum.
  • Gross autopsy findings dependent on underlying etiology:
    • Cortical necrosis:
      • Pale cortex, either total or patchy, with swollen parenchyma. Stops at corticomedullary junction.
      • Medulla normal or congested.
      • Infarctions have red (recent) or pale (few days) centers with hemorrhagic borders Renal infarct - pathology
    • Acute tubular necrosis:
      • Swelling.
      • Hyperemia.
      • Pallor of kidneys with mottled, flecked appearance (yellow areas of necrosis).
  • Ethylene glycol toxicity: gritty surface as scalpel cuts kidney tissue due to calcium oxalate.

Histopathology Findings

  • Dependent on underlying etiology of AKI:
    • Cortical necrosis:
      • Check for disseminated intravascular coagulopathy (stain for fibrin).
      • Areas of infarction.
      • Medulla may be spared.
    • Acute tubular necrosis:
      • Proximal convoluted tubules most affected (swelling, hydropic change or necrosis, inflammation).
      • Basement membrane may be intact in toxic damage, but not in ischemic damage.
      • Interstitial edema.
      • Calcium oxalate crystals in tubules with ethylene glycol.
      • May see casts in distal convoluted tubules Kidney oxalate nephrosis - crystal in tubules - pathology and collecting ducts.

Differential Diagnosis

  • Differentiate pre-renal, intrinsic renal and post-renal AKI.
  • Chronic renal failure (CRF) Kidney: chronic kidney disease (CKD) :
    • Usually chronic history of PU/PD which is not reported in AKI.
    • Kidneys small in CKD vs often normal to enlarged with AKI.
    • Low body condition, muscle condition expected with CKD.
    • Increased risk of non-regenerative anemia Anemia: non-regenerative with CKD.
    • Hyperkalemia more common in AKI but can be found in end-stage CKD.
    • Renal osteodystrophy identified in CKD.
    • PTH PTH assay concentrations elevated in CKD. Unlikely to be elevated in early stage AKI due to insufficient time for adaptation.
    • Carbamylated hemoglobin increased with CKD
  • Hypoadrenocorticism Hypoadrenocorticism : can present with acute collapse Collapse , isosthenuric urine, hyperkalemia.
    • ACTH stimulation test ACTH stimulation test required to differentiate.
    • Protracted hypovolemia and pre-renal AKI may ultimately result in intrinsic AKI Kidneys small in CKD vs often normal to enlarged with AKI.


Standard Treatment

  • Treat life-threatening complications (electrolyte derangements, eg hyperkalemia, metabolic acidosis, pH <7.1).
  • Remove access to underlying cause of AKI (toxins, drugs).
  • Treat underlying cause of AKI, eg Leptospirosis/pyelonephritis.
  • Fluid therapy Fluid therapy :
    • Correct pre-existing hypovolemia.
    • Correct pre-existing dehydration:
      • Provision of 5% body weight IVFT as cannot necessarily appreciate 5% body dehydration.
    • Provision of insensible losses.
    • Careful monitoring of 'in's and out's', body weight, hydration status, eg heart and pulse rate and quality, mucous membranes (color/capillary refill time/moisture), skin turgor.
  • If oliguria/anuria persists despite fluid therapy consider medical management for conversion of anuria/oliguria to polyuria:
    • Diuretic therapy:
    • Vasodilators:
      • Fenoldepam/dopamine Dopamine (limited evidence of benefit).
  • Renal replacement therapy:
    • Indications:
      • Inadequate urine output.
      • Life threatening pulmonary edema/fluid overload.
      • Hyperkalaemia or other life threatening metabolic disturbances, eg acid base status.
      • Progressive azotemia Azotemia.
      • Acute toxin/drug exposure, which may be dialyzable.
    • Modalities of renal replacement therapy:
      • Intermittent hemodialysis.
      • Continuous renal replacement therapy.
  • Supportive therapy:


  • Clinical examination:
    • Hydration and volume status: pulse/heart rate, mucous membrane color/capillary refill time/moisture, skin turgor, chemosis, nasal discharge.
    • Serial body weight measurement.
    • Oral ulceration.
    • Abdominal palpation for assessment of renal/abdominal pain.
  • Serum biochemistry: monitoring of azotemia, electrolytes (hyperkalemia, hyperphosphatemia, hypercalcemia, hyper/hyponatremia Hypernatremia Hyponatremia ).
  • Packed cell volume Hematology: packed cell volume /total protein Blood biochemistry: total protein.
  • Complete blood count: progression of anemia.
  • Urine output: placement of urinary catheter for monitoring of "ins and outs".
  • Blood pressure.
  • Venous blood gas: acid base status.
  • Central venous pressure Central venous pressure.

Subsequent Management


  • Continued treatment and supportive thearpy as outlined above.
  • If reach polyuric stage: high fluid therapy requirements best monitored and addressed through continued monitoring of hydration status, body weight and "ins and outs" with placement of urinary catheter.
  • If stabilizes with degree of renal recovery therapy in longer term for chronic kidney disease.


  • As above in acute stage.
  • If stabilizes with degree of renal recovery and enters chronic phase then treatment as for chronic kidney disease may be instigated.



  • If oliguria/anuria persists despite treatment.
  • If severe hyperkalemia occurs.
  • If severe metabolic acidosis occurs.
  • If azotemia continues to progress despite therapy.
  • Ethylene glycol poisoning Ethylene glycol poisoning.
  • If underlying cause is addressed early, renal failure may be reversible only if renal damage is not too extensive.

Expected Response to Treatment

  • Reslolution of anuria/oliguria - development of polyuria or ultimately normal urine output.
  • Azotemia decreases.
  • Hyperkalemia resolves.
  • Metabolic acidosis resolves.
  • Improvement of clinical signs (less lethargic, appetite improvement, less vomiting).

Reasons for Treatment Failure

  • Failure to increase urine production in oliguric/anuric patient.
  • Renal damage too severe.
  • Failure to recognize underlying cause early (ethylene glycol poisoning Ethylene glycol poisoning , infections).
  • Intractable hyperkalemia, acidosis or pulmonary edema without the option of dialysis.

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Eatroff A et al (2012) Long-term outcome of cats and dogs with acute kidney injury treated with intermittent hemodialysis: 135 cases (1997-2010). JAVMA 241 (11), 1471-1478 PubMed.
  • Geigy C A et al (2011) Occurrence of systemic hypertension in dogs with acute kidney injury and treatment with amlodipine besylate. J Small Anim Pract 52 (7) 340-346 PubMed.
  • Ross L (2011) Acute kidney injury in dogs and cats. Vet Clin North Am Small Anim Pract 41 (1), 1-14 PubMed.
  • Thoen M E & Kerl M E (2011) Characterization of acute kidney injury in hospitalized dogs and evaluation of a veterinary acute kidney injury staging system. J Vet Emerg Crit Care 21 (6) 648-657 PubMed.
  • Segev G et al (2008) A novel clinical scoring system for outcome prediction in dogs with acute kidney injury managed by hemodialysis. J Vet Intern Med 22 (2), 301-308 PubMed.
  • Yatsu T et al (1998) Effect of YM435, a dopamine DA1 receptor agonist, in a canine model of ischaemic acute renal failure. Gen Pharmacol 31 (5), 803-807 PubMed.
  • Tsuji Y et al (1993) An experimental model for unilateral ischemic acute renal failure in dog. Int Urol Nephrol 25 (1), 83-88 PubMed.
  • Nieto C G et al (1992) Pathological changes in kidneys of dogs with natural Leishmania infection. Vet Parasitol 45 (1-2), 33-47 PubMed.

Other Sources of Information