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Kidney: acute renal failure

ISSN 2398-2950


  • Syndrome with abrupt deterioration in renal function.
  • Cause: toxins/drugs, infection, renal ischemia.
  • Signs: uremia, oliguria (in most cases), anuria or polyuria (less commonly), dehydration, lethargy.
  • Treatment: prompt treatment to limit renal damage.
  • Prognosis: guarded, depending on unerlying cause; mortality may be high and extensive renal damage may result in chronic renal failure.

Presenting signs

  • Acute uremia Uremia:
    • Vomiting.
    • Diarrhea.
    • Anorexia.
    • Lethargy.
  • Oliguria (<0.5 ml/kg/h).
  • Oral ulceration, appears in 3-5 days.
  • Anuria.
  • Polyuria (>2 ml/kg/h) in mild cases or in recovery phase.
  • Abdominal pain in sublumbar region (depending on etiology).
  • Uremic encephalopathy (seizures) in very advanced cases.
  • Uremic pneumonitis (respiratory distress).

Acute presentation

  • Anuria.
  • Uremic crisis.

Geographic incidence

  • Leptospirosis is a cause of acute renal failure which has a geographical influence, eg Long Island of New York state in America.
  • Ethylene glycol toxicity Ethylene glycol poisoning more common in colder climates.

Cost considerations

  • If the owner can afford hemodialysis, it may improve survival and recovery rate. It is very expensive.
  • Intensive fluid therapy and monitoring is moderate to expensive.
  • Acute renal failure is rarely responsive to inexpensive therapy.

Special risks


  • Hyperkalemia Hyperkalemia and metabolic acidosis (pH <7.1) Acid base imbalance can cause severe cardiac problems and exacerbate neurological signs.
  • Overdosage of drugs, since most drugs have some degree of renal clearance.



Acute tubular necrosis

Pre-renal ARF

Post-renal ARF

Predisposing factors


  • Pre-existing renal damage with additional insult, eg reduced renal perfusion.
  • Any cause of reduced renal blood flow.


  • Anesthesia, especially without appropriate blood pressure monitoring and IV fluid support.
  • Chemotherapy with cisplatin.
  • Access to antifreeze (ethylene glycol).
  • Misuse of NSAIDs, aminoglycosides, diuretics or vasodilators.


Four phases

  • Initiation phase (renal insult resulting in damage to renal parenchyma; injury potentially reversible at this stage; hours to 1-2 days).
  • Extension phase (ongoing cellular injury progressing to cell death, with progressive decline in GFR and loss of urine concentrating ability).
  • Maintenance phase (elimination of inciting factors at this stage does not alter existing damage or rate of recovery; signs of uremia may be present; a prolonged maintenance phase is associated with slower recovery and increased likelihood of permanently reduced renal function).
  • Recovery phase (progressive return of renal function).
  • Reduced renal blood flow   →   reduced oxygen and energy transport to cells   →   cell swelling and membrane damage   →   vasoconstriction and inflammatory mediator release   →   further vasoconstriction.
  • Nephrons are damaged at different sites (glomerulus, tubular cell, intercellular junction, basement membrane) depending on etiology   →   acute decline in glomerular filtration rate   →   increased urea/creatinine, decrease in urine specific gravity   →   uremic signs, oliguria (sometimes anuria or polyuria), fluid and electrolyte imbalances, acidosis.


  • Animals may die acutely, especially if underlying cause is not detected and treated or if oliguric phase persists.
  • If treated appropriately, animals may recover, but recovery phase can take >3 weeks of intensive care.


Presenting problems

  • Vomiting Vomiting.
  • Anorexia.
  • Oliguria (less common, anuria or polyuria).
  • Shock.
  • Neurological signs.

Client history

  • Lethargy.
  • Anorexia.
  • Vomiting.
  • Diarrhea.
  • Oliguria/anuria.
  • Exposure to drugs/toxins.
  • Polyuria/polydipsia (may suggest chronic renal failure pre-existing).
  • Neurological signs.
  • Halitosis.

Clinical signs

  • Enlarged kidneys (may be small if superimposed on chronic renal failure).
  • Oral ulceration, halitosis.
  • Bradycardia if severe hyperkalemia.
  • Bradycardia, hypothermia, dehydration - evidence of shock.
  • Melena.
  • Abdominal pain (sublumbar).
  • Pyrexia.

Diagnostic investigation




  • Isosthenuria SG <1.020 if urine being produced (unless pre-renal element to acute renal failure).
  • Ca-oxalate crystalluria Urinalysis: calcium oxalate crystal (ethylene glycol poisoning).
  • Abnormal sediment examination Urinalysis: centrifuged sediment (cells, casts) especially with pyelonephritis.
  • Proteinuria Proteinuria, hematuria Hematuria depending on etiology.




  • See ultrasonography of the kidneys Ultrasonography: kidney.
  • Enlarged kidneys.
  • Bright (hyperechoic) renal cortex in ethylene glycol cases.


  • Only indicated if no response to therapy or if prognosis essential.
    Biopsy may cause hemorrhage resulting in further compromise of renal function.
  • Renal histopathology may identify underlying cause of acute renal failure and extent of renal damage.
    Do not biopsy if infectious process is suspected.Do not biopsy if bleeding diathesis is severe; assess with coagulation profile and buccal mucosal bleeding time.


  • See ECG overview ECG: overview and principles of interpretation ECG: principles of interpretation.
  • Changes are usually from hyperkalemia.
  • If severe hyperkalemia, may show:
    • Tall T waves.
    • Wide QRS complex and prolonged PR interval.
    • Absent P waves.

Confirmation of diagnosis

Discriminatory diagnostic features

  • History.
  • Signs.
  • Biochemistry.
  • Urinalysis.
  • Radiography/ultrasound.

Definitive diagnostic features

  • Renal biopsy.

Gross autopsy findings

  • Ethylene glycol nephrosis:
    • Gritty surface as scalpel cuts kidney tissue due to calcium oxalate.
  • Enlarged kidneys.
  • Small volume of urine in bladder.

Histopathology findings

  • Calcium oxalate crystal in tubules with ethylene glycol.
  • Evidence of underlying pathology on renal biopsy (toxic change, ischemic change, infection).

Differential diagnosis

Chronic renal failure (CRF)

  • See chronic renal failure for possible differentials Kidney: chronic kidney disease:
    • No history of PU/PD in acute renal failure (ARF).
    • Usually large or normal sized kidneys in ARF, small kidneys in CRF.
    • No anemia in ARF, unless there is concurrent vasculitis or bleeding diathesis.
    • Increased potassium more common in ARF.
    • No osteopenia in ARF.
    • CRF patients more likely to have poor body condition, whereas ARF patients more likely to be in good body condition.
    May have ARF superimposed on chronic.

Prerenal azotemia

  • Dehydration, hemorrhage, shock, hypoperfusion of kidneys.
  • Hypersthenuric urine.

Post-renal azotemia

  • Usually due to physical obstruction Uremia: hyperkalemia, anuria, azotemia.
    Look for evidence of urinary tract obstruction or urinary tract rupture.


Initial symptomatic treatment

  • H2-receptor blockers, eg cimetidine Cimetidine (2.5-5.0 mg/kg BID-TID), ranitidine  Ranitidine (0.5-2.0 mg/kg BID).
  • Gastrocytoprotective drugs Therapeutics: gastrointestinal system 
  • Broad-spectrum antibiotics to prevent infections (animals in ARF are predisposed to infections) but care if indwelling urinary catheter is placed to measure urine output, as more likely to develop resistant urinary tract infection..
  • Anti-emetics - start with metoclopramide Metoclopramide. If ineffective consider low doses of prochlorperazine.
  • Nutritional support with high caloric density diet Dietetic diet: for convalescence (animal is in a catabolic state). Consider naso-esophageal, pharyngostomy or percutaneous gastrostomy tube.

Standard treatment

  • Treat life-threatening complications:
    •  Hyperkalemia Blood biochemistry: potassium - can give 10% calcium gluconate  Calcium gluconate 0.5-1 ml/kg IV over 15 min as cardiac protectant; followed by insulin and glucose saline.
    • Metabolic acidosis (pH <7.1) - consider use of sodium bicarbonate.
  • Treat underlying cause of ARF (infection, toxins).
  • Fluid therapy Fluid therapy: overview Hartman's or saline if hyperkalemic to correct dehydration and cause diuresis. Level of fluid therapy needs to be adjusted to urine output to prevent overhydration.
    Weigh animal before fluid therapy and can safely increase bodyweight by 3-5% with fluids since dehydration up to 5% is not clinically detectable once rehydrated.
  • If oliguria persists despite rehydration, administer loop diuretics, eg frusemide   Furosemide  2-4 mg/kg.
  • Consider use of low dose dopamine 2-5 microg/kg/min in 5% dextrose Dopamine or mannitol infusion Mannitol (1-2 mg/kg/min), however little evidence to support efficacy.
  • If oliguria/anuria persists despite these treatments, peritoneal dialysis or hemodialysis is indicated (instill 7.5 ml of 50% dextrose into 250 ml Hartman's and give intraperitoneally and remove 6 hours later).
  • Fluid replacement should match output. Ideally indwelling urinary catheter should be attached to closed collection system in order that 'ins and outs' can be matched (+ 20 ml /kg/day for insensible losses). 
  • Post-oliguria diuresis may require high fluid levels for 48-72 hours, then fluids should be tapered gradually over several days once patient eating.


  • Urine output (should be >0.5 ml/kg/h); once patient rehydrated match fluid input to urine output plus insensible losses (20 ml/kg/day).
  • Clinical hydration.
  • PCV/total protein.
  • Serial central venous pressures (to prevent overhydration) Central venous pressure.
  • Serial bodyweights (to monitor overhydration).
  • Biochemistry: urea, creatinine, serum potassium.
  • Blood gas (level of acidosis).

Subsequent management



  • Same as chronic renal failure if extensive damage has been done to kidneysKidney: chronic kidney disease.
  • Reculture urine in case of pyelonephritis.



  • Vaccination against Leptospirosis will not prevent all serovars. Not routinely performed in cats due to low level of clinical disease.
  • Fluid therapy (surgery, anesthesia, thromboembolic disease, dehydration) to prevent renal underperfusion.
  • Monitor urine for tubular casts during aminoglycoside therapy.
  • Monitor BUN/creatinine during therapy with:




  • 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.


  • If underlying cause is addressed early, renal failure may be reversible, only if renal damage is not too extensive.
  • Patients may require ongoing therapy for chronic kidney disease.

Expected response to treatment

  • Urine production increases within first 48 hours.
  • Azotemia decreases.
  • Hyperkalemia resolves.
  • Metabolic acidosis resolves.
  • Improvement of clinical signs.
  • Renal function may improve over 10-14 days.

Reasons for treatment failure

  • Failure to increase urine production in oliguric patient.
  • Renal damage too severe.
  • Failure to recognize underlying cause early (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.
  • Dorval P & Boysen S R (2009) Management of acute renal failure in cats using peritoneal dialysis: a retrospective study of six cases (2003-2007). J Feline Med Surg 11 (2), 107-115 PubMed.
  • Worwag S & Langston C E (2008) Acute intrinsic renal failure in cats: 32 cases (1997-2004). JAVMA 232 (5), 728-732 PubMed.
  • Sigrist N E (2007) Use of dopamine in acute renal failure. J Vet Emerg Crit Care 17 (2), 117-126 VetMedResource.
  • Stokes J E & Forrester S D (2004) New and unusual causes of acute renal failure in dogs and cats. Vet Clin North Am Small Anim Pract 34 (4), 909-922 PubMed.
  • Grauer G F (1998) Fluid therapy in acute and chronic renal failure. Vet Clin North Am Small Anim Pract 28 (3), 609-622 PubMed.
  • Grauer G F (1996) Prevention of acute renal failure. Vet Clin North Am Small Anim Pract 26 (6), 1447-1459 PubMed.
  • Ohashi F, Awaji T, Shimada T et al (1995) Plasma methylguanidine and creatinine concentrations in cats with experimentally induced acute renal failure. J Vet Med Sci 57 (5), 965-966 PubMed.
  • Mealey K L, Boothe D M (1994) Nephrotoxicosis associated with topical administration of gentamicin in a cat. JAVMA 204 (12) 1919-1921 PubMed.

Other sources of information

  • Langston C (2010) Acute Uraemia. In:T extbook of Veterinary Internal Medicine7th edn. Ettinger S J & Feldman E C (eds). W B Saunders, pp 1969-1985.
  • Chew D J & Gieg J A (2006) Fluid therapy during intrinsic renal failure. In: Fluid, Electrolyte and Acid-base Disorders in Small Animals. Di Bartola S P (ed). W B Saunders, pp 518-540.
  • Frenier S L & Dhein C R (1991) Diagnosis and management of acute renal failure. In: Consultations in feline internal medicine 1. (ed) J R August. W B Saunders. pp 281-288.