Acute Renal Failure 2006

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STANDARDS of CAREEMERGENCY AND CRITICAL CARE MEDICINE

VOL 8.4MAY 2006

FROM THE PUBLISHER OF COMPENDIUM

DIAGNOSTIC CRITERIA

Historical InformationGender/Age/Breed Predisposition None.

Owner ObservationsAcute onset (hours to several days) of clinical signs,which may vary depending on the cause of ARF:

Depression, lethargy, weakness. Anorexia, vomiting, diarrhea.

Change in urine production:

Usually decreased.

Increased urine production (polydipsia/poly-uria) is much less common and tends to be ofshort duration.

Ataxia, seizures.

Other Historical Considerations/Predispositions Exposure or potential exposure to toxic sub-

stances, including drugs (see box on page 4).

Seasonal and environmental conditions conduciveto exposure to infectious diseases.

Recent or concurrent severe illness that couldresult in ischemia, sepsis, and/or multiple organdysfunction syndrome.

Peer Reviewed

10 Anemia as a Manifestation of Malignancy

Also in this issue:

1

ACUTE RENAL FAILURELinda A. Ross, DVM, MS, DACVIM (Small Animal Internal Medicine)Associate ProfessorDepartment of Clinical SciencesCummings School of Veterinary MedicineTufts University

Questions? Comments? Email [email protected],fax 800-556-3288, or post on the Feedback page atwww.SOCNewsletter.com.

Acute renal failure (ARF) is characterized by therapid loss (over hours to several days) ofnephron function, resulting in azotemia and

fluid, electrolyte, and acidbase abnormalities.Although obstruction to urine flow or rupture of theurinary tract can cause renal failure that occurs withina short time (postrenal failure), this article covers onlyARF due to intrinsic disease of the renal parenchyma.

Clinically, ARF is divided into three stages. The first

(initiation) occurs during and immediately following theinsult to the kidneys, when pathologic damage to thekidneys is occurring. This phase usually lasts less than48 hours, during which time clinical and laboratoryabnormalities may not be apparent. The second stage(maintenance) is characterized by azotemia and/or ure-mia and may last for days to weeks. Oliguria (


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M A Y 2 0 0 6 V O L U M E 8 . 42

STANDARDS of CAREEMERGENCY AND CRITICAL CARE MEDICINE

MAY 2006 VOL 8.4

Editorial Mission:

To provide busy practitioners with concise,peer-reviewed recommendations on currenttreatment standards drawn from publishedveterinary medical literature.

This publication acknowledges that standardsmay vary according to individual experience

and practices or regional differences. Thepublisher is not responsible for author errors.

Compendiums Standards of Care:

Emergency and Critical Care Medicine

is published 11 times yearly(January/February is a combined issue)by Veterinary Learning Systems,

780 Township Line Road, Yardley, PA 19067.

The annual subscription rate is $83.

For subscription information, call

800-426-9119, fax 800-589-0036,

email [email protected], or visit

www.SOCNewsletter.com. Copyright

2006, Veterinary Learning Systems.

Editor-in-ChiefDouglass K. Macintire, DVM, MS,

DACVIM, [email protected]

Group PublisherRay [email protected]

Editorial, Design, and ProductionLilliane Anstee, Vice President,

Editorial and Design

Maureen McKinney, Editorial Director

Cheryl Hobbs, Senior Editor

Michelle Taylor, Senior Art Director

Bethany L. Wakeley, Studio Manager

Chris Reilly, Assistant Editor

Kristin Sevick, Editorial Assistant

Andrea Vardaro, Editorial Assistant

Editorial Review BoardMark Bohling, DVMUniversity of Tennessee

Harry W. Boothe, DVM, DACVSAuburn University

Derek Burney, DVM, PhD, DACVIM

Houston, TXJoan R. Coates, DVM, MS, DACVIMUniversity of Missouri

Curtis Dewey, DVM, DACVIM, DACVSPlainview, NY

Nishi Dhupa, DVM, DACVECCCornell University

D. Michael Tillson, DVM, MS, DACVSAuburn University

KEY TO COSTS

$ indicates relative costs of any diagnostic and treatment regimens listed.$ costs under $250$$ costs between $250 and $500$$$ costs between $500 and $1,000$$$$ costs over $1,000

Physical Examination Findings Normal body condition.

Bilaterally normal to enlarged kidneys that may be painful when pal-pated; however, normal renal palpation does not rule out ARF.

Signs of dehydration:

Decreased skin turgor.

Dry or tacky mucous membranes.

Signs of hypovolemia:

Slow capillary refill time.Tachycardia.

Weak pulses.

Hypothermia.

Depression, lethargy, weakness.

Uremic breath.

Oral ulceration and/or necrosis of the tongue.

Laboratory Findings $ Elevated blood urea nitrogen (BUN; normal, 1025 mg/dl) and serum

creatinine (normal, 1.02.0 mg/dl) concentrations.

Dilute urine (specific gravity [SG] < 1.030 in dogs and < 1.035 in cats)concurrent with azotemia. Some animals with less severe renal injurylose the ability to concentrate urine but do not become azotemic.

Normal to elevated serum potassium concentration (normal, 3.55.5mEq/L).

Metabolic acidosis.

Hyperphosphatemia (normal, 3.06.3 mg/dl).

Hypocalcemia (normal total calcium, 9.511.5 mg/dl; normal ionizedcalcium, 1.171.38 mmol/L).

Usually mild to moderate.

May be severe in association with marked hyperphosphatemia or in

animals with ethylene glycol intoxication. Hematocrit may be normal to elevated, consistent with dehydration.

Leukogram may reflect the underlying disease causing ARF (e.g., leuko-cytosis with pyelonephritis).

Coagulation profile may reflect the underlying disease causing ARF (e.g.,thrombocytopenia with leptospirosis).

Other Diagnostic FindingsRadiography $ Normal to enlarged kidneys.

Absence of radioopaque uroliths.

Ultrasonography $$$ Normal to enlarged kidneys.

May show increased echogenicity and loss of corticomedullary distinction.


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A hyperechoic band at the corticomedullary junc-tion has been seen with ethylene glycol toxicityand other causes of ARF; however, it has also beenseen in normal dogs and cats, and therefore its sig-nificance is unknown.

Other $$$Tests to rule out specific causes of ARF may be per-

formed, depending on such factors as the patientsspecies (dog or cat), geographic location, season, andpotential for exposure.

Ethylene glycol poisoning:

Serum level.

Severe metabolic acidosis (normal arterialblood pH, 7.367.44) with increased anion gap(anion gap = [serum Na + K] [serum bicar-bonate + Cl]; normal, 1225 mEq/L).

Increased serum osmolar gap (osmolar gap =measured serum osmolality calculated serumosmolality; normal, 1.030; cats, SG >

1.035) in conjunction with azotemia.

STANDARDS ofCARE: E M E R G E N C Y A N D C R I T I C A L C A R E M E D I C I N E3

Rapid resolution of azotemia with appropriatefluid therapy and correction of dehydration.

Postrenal Azotemia $$$Obstruction Urethral:

Historical and/or physical examination findingsof stranguria, dysuria, hematuria, and inability

to urinate.Inability to pass a urinary catheter.

Radiographic or ultrasonographic evidence ofobstructing urolithiasis or tissue masses.

Ureteral urolithiasis:

Appears to be occurring with increasing fre-quency, especially in cats; therefore, all catswith ARF should be evaluated for ureteralurolithiasis.

Radiographic or ultrasonographic evidence ofobstructing urolithiasis.

Rupture of a Portion of the Urine Collecting System History or possibility of trauma.

Ultrasonography or contrast radiography to iden-tify location of rupture.

Chronic Renal Failure $$$ Epidemiology: If the animal is young, familial

renal disease should be considered if it has beenreported in the breed in question.

History: Signs of several weeks duration or longer:

Polydipsia/polyuria.Weight loss.

Decreased appetite.

Vomiting.

Animals with chronic disease may experienceacute exacerbations of clinical signs of renalfailure or even oliguria or anuria.

Physical examination:

Poor body condition.

Pale mucous membranes.

Small kidneys on palpation.

Rarely, rubber jaw (flexible mandible) due torenal secondary hyperparathyroidism.

Laboratory data:

Normocytic, normochromic anemia.

Hypoalbuminemia in animals with protein-losing nephropathies.

Imaging: Small, irregular kidneys.

Histopathology: Confirmation of chronic disease.

Hypoadrenocorticism $$ Corticotropin stimulation test.


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M A Y 2 0 0 6 V O L U M E 8 . 44

TREATMENTRECOMMENDATIONS

Initial TreatmentThe dose of drugs that are excreted primarily in urineneeds to be reduced in proportion to the degree ofazotemia. These drugs are noted with an asterisk (*).The following measures are indicated in most patients:

Intravenous fluid therapy is the mainstay of ther-apy in most patients (see box on page 5): Place-ment of a jugular catheter ($) allows monitoring of

central venous pressure, which can be beneficialin adjusting fluid therapy. However, if hemodialy-sis is a therapeutic option, the jugular veins shouldbe preserved for placement of a hemodialysiscatheter and peripheral IV catheters should beused instead for initial fluid therapy.

Hyperkalemia should be corrected if present (seebox on page 5). $

Placement of an indwelling urinary catheter tomonitor urine output should be considered, butpotential benefit should be weighed against the riskof inducing an ascending urinary tract infection. $

Specific Treatment ofUnderlying Cause (If Identifiedor Strongly Suspected)Ethylene Glycol Intoxication Emesis should be induced if ingestion of ethylene

glycol occurred within 3 hours of presentation andthe animal is not obtunded.

Antidote should be administered if the patient isnot yet azotemic.

Ethanol 20%: 5.5 ml/kg IV q4h for five treat-ments, then q6h for four treatments. $

OR

Ethanol 30%: 1.3 ml/kg IV bolus, then 0.42ml/kg/hr IV for 48 hours. $

OR

4-Methylpyrazole (dogs only): 20 mg/kg IVthen 15 mg/kg IV at 12 and 24 hours, then 5mg/kg IV at 36 hours. $$$

Diuresis should be induced with IV fluids. $$

Hemodialysis: Both intact ethylene glycol andsome of its metabolites can be removed byhemodialysis. $$$$$$$

Leptospirosis In endemic areas, leptospirosis should be consid-

ered as a differential diagnosis in all dogs withrenal failure of unknown cause; treatment shouldbe instituted immediately.

Initial antibiotic therapy for 2 weeks to eliminate

leptospiremia: $Penicillin*: 25,00040,000 U/kg IV, SC, or IM

bid.

Ampicillin*: 22 mg/kg IV or SC tid.

Amoxicillin*: 22 mg/kg PO bid.

Doxycycline: 5 mg/kg PO or IV bid.

Subsequent antibiotic therapy for 2 weeks to elim-inate renal carrier state: $

Doxycycline: 5 mg/kg PO or IV bid.

Tetracycline*: 22 mg/kg PO tid.

Azithromycin: 20 mg/kg PO sid.

COMMON CAUSES OFACUTE RENAL FAILUREIN DOGS AND CATS

Ischemia

Infarction

Toxins Ethylene glycol

Heavy metals

Organic compounds

DrugsAminoglycoside antibioticsAmphotericin BCisplatinNSAIDsRadiographic contrast agents

Grapes or raisinsa

Hemoglobinuria/myoglobinuria

Lily plantb

Envenomation (e.g., snake, bee, wasp, bull ant)

Infectious diseases Pyelonephritis

Leptospirosisa

Hypercalcemia Calciferol-containing rodenticides

Human dermatologic preparations containingvitamin D analogs

Paraneoplastic syndrome (e.g., associated withlymphoma or apocrine gland adenocarcinoma ofthe anal sac)

Hyperviscosity Hyperglobulinemia

Polycythemia

Multiple organ dysfunction syndrome

Sepsis

Acute pancreatitis

aReported only in dogs.bReported only in cats.


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FLUID THERAPY AND ELECTROLYTEMANAGEMENT FOR ANIMALS WITH ARF

Intravenous Fluid Therapy Type of fluid:

Lactated Ringers solution (in patients that are nothyperkalemic).

Potassium-free fluid (e.g., 0.9% sodium chloride or0.45% sodium chloride in 2.5% dextrose) inhyperkalemic patients or if serum potassium cannotbe immediately measured.

Fluid volume calculation:

Replacement of deficit: % dehydration bodyweight (kg) 1,000 = ml fluid deficit. Deficitshould be replaced over 46 hr to correcthypovolemia and improve renal blood flow.(NOTE: This rate replaces fluid deficits more rapidlythan is normally recommended, which is indicatedin patients with renal failure to restore renal bloodflow.) An initial bolus of up to 90 ml/kg may benecessary in animals that are severely volumedepleted.

Maintenance: 66 ml/kg/24 hr.Volume to compensate for ongoing losses via the

gastrointestinal tract (estimate volume) and/orpolyuria (measure urine output).

Frequent monitoring of volume and hydration status(by clinical assessment and measurement of centralvenous pressure) and urine production andappropriate adjustment of IV fluidsare critical.

Special Considerations for Oliguric or Anuric Patients Following replacement of volume deficits, urine flow

should rapidly increase to 25 ml/kg/hr.

If urine production is inadequate, the patientscirculating blood volume should be reassessed.

Additional IV fluids should be administered if theanimal is hypovolemic.

If the animal has normal to increased circulatingvolume:

The rate of fluid administration should be decreased.

An indwelling urinary catheter should be placed(if not already done).

Fluids should be administered by calculatingins and outs to match urine output:Maintenance fluid requirement is calculatedfor a short interval (e.g., 4 hr), and volume of

urine produced during the previous interval isadded to the maintenance amount to calculatethe volume of IV fluids to be administered overthe subsequent interval.

If these measures are not successful in restoring urineoutput within 6 to 12 hours, the next therapeutic stepis peritoneal dialysis or hemodialysis; if hemodialysisis not available or the owners are unwilling to pursueit, euthanasia should be considered.

Treatment of Severe Hyperkalemia (>8.0 mEq/L)NOTE: Specific therapy is indicated in patients with severehyperkalemia; fluids alone may be sufficient in patientswith mild to moderate hyperkalemia. The decision

whether to administer sodium bicarbonate, dextrose, orinsulin and dextrose initially appears to be a clinicaljudgment that varies among specialists and institutions.

Sodium bicarbonate: 0.52 mEq/kg IV over 1520 minto effect.

Insulin and glucose:

Regular insulin (2.2 U/kg) added to a 250-ml bag of2.5% dextrose; administered at 510 ml/hr.

OR

Regular insulin (0.51.0 U/kg) and glucose (2 g/Uof insulin) added to IV fluids.

OR

Regular insulin (0.250.5 U/kg) and glucose (2 g/Uof insulin) diluted to a 5% to 10% solution and givenby IV push; followed with 2.5% dextrose in IV fluids.

Calcium gluconate: 0.51.0 ml/kg 10% calciumgluconate IV over 1015 min in very severe cases;should be avoided in animals with hypercalcemia.NOTE: Recommended dose varies among specialists.

Drugs that are ineffective in clearing the renalcarrier state include chloramphenicol, sulfon-amides, and fluoroquinolones.

Pyelonephritis Antibiotic therapy should be based on culture and

sensitivity testing of urine or renal tissue.

Antibiotic used should be nonnephrotoxic and pri-marily excreted by the kidneys.

Duration of therapy is typically 4 to 8 weeks.

Alternative/OptionalTreatments/Therapy If oliguria (urine output < 1 mg/kg/hr) or anuria

occurs after the animal is adequately hydrated and


receiving appropriate fluid therapy, measures shouldbe instituted to try to increase urine output (see boxon page 7). It is important to recognize that

increased urine output is not necessarily associatedwith improvement in renal blood flow or glomerularfiltration rate. The goal is to permit continued fluidtherapy and medical management in the hope thatthe kidneys will be able to repair the renal damage.

If the measures discussed in the box on page 7 arenot successful in restoring urine output within 6 to12 hours, the next therapeutic step would beeither peritoneal dialysis or hemodialysis; ifhemodialysis is not available or the owners areunwilling to pursue it, euthanasia should be con-sidered. Detailed descriptions of dialysis are


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M A Y 2 0 0 6 V O L U M E 8 . 46

beyond the scope of this article. $$$$

If the animal improves and enters the recovery

phase of ARF, marked polyuria can result in fluidand/or electrolyte deficits. Frequent monitoring(Table 1) and adjustment of fluid volume and typeare necessary.

Supportive TreatmentUremia will result in a number of pathophysiologicabnormalities, including vomiting, metabolic acidosis,arterial hypertension, and malnutrition. Therapy toalleviate these abnormalities should be tailored to theneeds and response of the individual animal.

Treatment for VomitingGastric Protectants $ H2 receptor antagonist:

Famotidine* (Pepcid, Merck & Co.): 0.51mg/kg PO, SC, IM, or IV sidbid.

Proton pump inhibitors:

Omeprazole* (Prilosec, Procter & Gamble): 0.7mg/kg PO sid.

Lansoprazole (Prevacid, TAP PharmaceuticalProducts): 0.61.0 mg/kg IV sid.

Pantoprazole* (Protonix, Wyeth Pharmaceuti-

cals): 1040 mg IV slowly over 15 minutes sidOR0.71 mg/kg IV sid.

Antiemetics $ Metoclopramide* (Reglan, Schwarz Pharma or

Baxter Heathcare): 0.10.5 mg/kg PO, IM, SQ, orIV tidqid OR 12 mg/kg/day CRI.

Dolasetron* (Anzemet, Sanofi-Aventis): 0.6 mg/kgPO or SQ sid ORdrug can be diluted in compati-ble IV fluid and administered over 15 min sid.

Ondansetron (Zofran, GlaxoSmithKline): 0.10.2mg/kg SQ tid OR 0.5 mg/kg IV loading dose and

then 0.5 mg/kg/hr CRI.

Chlorpromazine: 0.20.5 mg/kg SQ, IM, or IV tid

qid. May cause sedation.

Treatment of Metabolic Acidosis IV fluid therapy may be sufficient for patients with

mild to moderate acidosis; treatment should beconsidered if blood pH is below 7.2 or serumbicarbonate is less than 14 mEq/L after correctingfluid deficit.

Calculation of bicarbonate deficit: Body weight(kg) 0.3 (24 measured bicarbonate) = mEq ofbicarbonate to replace.

One-quarter of the total bicarbonate deficit shouldbe given as sodium bicarbonate (IV) in the first 12hours; the patient should then be reevaluated. Fur-ther bicarbonate can be administered if indicated,but a conservative approach should be used.

Sodium bicarbonate is incompatible with lactatedRingers solution.

Complications of sodium bicarbonate therapyinclude paradoxic cerebrospinal fluid acidosis,decreased ionized serum calcium, and hyperna-tremia.

The total bicarbonate deficit should be replaced

over 48 hours, if necessary.

Treatment of Arterial Hypertension $Treatment may be limited because the vomiting asso-ciated with uremia often precludes oral medication,and most antihypertensive drugs are available only inoral formulations.

Dogs Amlodipine (Norvasc, Pfizer): 0.10.25 mg/kg PO

sidbid.

Angiotensin-converting enzyme (ACE) inhibitors;

Frequency of Measurement (hr)

Parameter Nonoliguric Oliguric/Anuric Polyuric

BUN and serum creatinine 2448 1224 2448

Serum sodium, potassium, and chloride 24 68 1224

Acidbase status 2448 812 Hematocrit and total solids 1224 1224 1224

Blood pressure 1224 812 24

Body weight 12 812 1224

Urine production As the animal voids 24 68

Clinical assessment of hydration, including 12 68 1224lung auscultation

Central venous pressure 68 46 812

T A B L E 1P a t i e n t M o n i t o r i n g d u r i n g H o s p i t a l i z a t i o n


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TREATMENT OFOLIGURIA OR ANURIA

1. An indwelling urinary catheter should be placedto monitor urine output.

2. Drugs should be administered to increase urineoutput. These agents can be administered indifferent sequence, serially, or in combination,depending on the judgment of the veterinarian. If

urine output does not increase within 612 hours,dialysis should be considered.

Diuretic therapy:

Furosemide: 2 mg/kg IV bolus; if effective,diuresis usually begins within 1530 min.

Dose should be increased at hourly intervalsto 46 mg/kg if initial dose does not inducediuresis.

In normal dogs, CRI has been shown to bemore beneficial than intermittent dosing inincreasing urine production: 0.66 mg/kg IVbolus followed by 0.66 mg/kg/hr CRI; someclinicians recommend a dose of 0.51.0mg/kg/hr CRI.

Osmotic diuresis:

Mannitol 20%: 0.51 g/kg IV bolus slowlyfollowed by either 1.02.0 mg/kg/min CRIor repeat boluses q46h at a dose of0.250.5 g/kg.

Contraindicated in animals with fluidoverload, pulmonary edema, or congestiveheart failure.

Dopamine infusion:

At low doses (0.53 g/kg/min), dopaminehas been used to stimulate dopamine DA1

receptors, induce smooth muscle relaxation,decrease renal vascular resistance, increaserenal blood flow, and induce natriuresis.

Controversial; see Checkpoints

3. Treat hyperkalemia (see box on page 5).

ACE inhibitors have been reported to be associ-ated with increases in BUN and creatinine in asmall percentage of dogs.

Enalapril* (Enacard, Merial): 0.250.5 mg/kg

PO or IV sidbid.Benazepril (Lotensin, Novartis): 0.250.5mg/kg PO sid.

Both an ACE inhibitor and amlodipine can beadministered if necessary.

Cats Amlodipine: 0.6251.25 mg PO sid.

Severe Hypertension $ Hypertension severe enough to cause clinical con-

sequences may require more aggressive therapy.

Nitroprusside infusion should be considered, but

administration must be performed in an intensivecare unit setting with close monitoring,

0.51.0 g/kg/min IV.

Dose is increased by 0.51 g/kg/min every 5min until desired blood pressure is attained.

Rapid or marked decreases in blood pressure thatmay affect renal blood flow must be avoided.

Nutritional Support $$$ Parenteral nutrition is indicated initially until the

animal is no longer vomiting.

Enteral nutrition using a feeding tube (naso-

esophageal, esophagostomy, or gastrostomy) canbe used when the animal is not vomiting and cantolerate sedation or anesthesia necessary for tubeplacement.

Patient MonitoringParameters to be monitored include BUN, serum cre-atinine, electrolytes, blood gas, hematocrit and totalsolids, arterial blood pressure, body weight, clinicalassessment of hydration, central venous pressure, andurine production. Frequency of monitoring dependson the severity of uremia and stage of ARF (Table 1).

Home Management Animals must not be discharged until renal func-

tion returns to normal or until they are stable andno longer showing signs of uremia.

Management recommendations depend on theinciting cause of ARF, if identified, and the degreeof resolution of azotemia at the time the patient isdischarged from the hospital.

Future exposure to nephrotoxic substances must beavoided and exposure to infectious agents minimized.

The drugs used to stimulate urineproduction in animals with oliguria oranuriafurosemide, mannitol, anddopaminemay be administered in adifferent sequence, sequentially, or incombination, depending on the judgmentof the veterinarian.

Dopamine infusion for treatment of oliguriaor anuria is controversial. In humans, it isno longer recommended for use in ARFbecause studies have failed to show anybenefit in preventing ARF in at-risk patientsor in reducing mortality in patients withestablished ARF.

C H E C K P O I N T S



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M A Y 2 0 0 6 V O L U M E 8 . 48

Animals should always have free access to freshdrinking water.

Animals with pyelonephritis:

Antibiotic therapy for a minimum of 4 to 8weeks.

Urine culture and sensitivity testing should beconducted 1 to 2 weeks after completion ofantibiotic therapy and every 3 to 6 monthsthereafter.

Animals with residual renal dysfunction should bemanaged for chronic renal failure; a discussion ofthese measures is beyond the scope of this article.a

Milestones/Recovery Time Frames Recovery from ARF may take days, weeks, or

months; it is impossible to predict in any givenpatient.

Recovery is characterized by decreasing BUNand serum creatinine, normalization of elec-trolytes and acidbase status, improvement inurine concentrating ability, and resolution of signsof uremia.

Hospitalization and IV fluid therapy is recom-mended until BUN and serum creatinine levelsreturn to normal or plateau for 3 to 5 days. If theanimal is eating, drinking, and maintaining hydra-

tion even though it is still azotemic, dischargingthe patient and allowing the owners to manage itat home should be considered.

Treatment Contraindications Administration of nephrotoxic drugs, such as

aminoglycoside antibiotics or NSAIDs.

Excessive fluid administration resulting in overhy-dration.

Medication or other treatment that results inhypotension.

O N T H E N E W S F R O N T

Renal transplantation may be consideredfor cats with ARF and uremia that fail toimprove with therapy or for those witholiguria or anuria. Dialysis may benecessary to stabilize the cat beforetransplantation. $$$$

Renal transplantation has not had a highsuccess rate in dogs; however, at least oneinstitution (Auburn University) is nowoffering renal transplants for select caninepatients. $$$$

Continuous renal replacement therapy(CRRT) may be an alternative to standardhemodialysis for dogs and cats. $$$$

The concept behind CRRT is to performdialysis in a more physiologic way,

slowly, over 24 hours. CRRT minimizes effects of fluid and

electrolyte shifts.

CRRT may be particularly beneficial insmaller patients (cats and dogsweighing


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PROGNOSIS

Favorable Criteria The cause of ARF is one that responds well to

appropriate therapy (e.g., pyelonephritis, lep-tospirosis).

Rapid improvement in azotemia with appropriatetherapy.

Absence of concurrent systemic disease.

Unfavorable Criteria Cause of ARF is one that has historically been

associated with poor prognosis (e.g., ethylene gly-col intoxication).

Oliguria or anuria.

Severe azotemia (serum creatinine > 10 mg/dl).

Lack of improvement or worsening of azotemiawith appropriate fluid and supportive therapy.

Concurrent systemic disease, such as pancreatitisor sepsis.

RECOMMENDED READING

Cowgill LD, Francey T: Acute uremia, in Ettinger SF, Feldman EC(eds): Textbook of Veterinary Internal Medicine, ed 6. St. Louis,

Elsevier Saunders, 2005, pp 17311751.

Dzyban LA, Labato MA, Ross LA, Murtaugh RJ: Peritoneal dialysis:A tool in veterinary critical care. J Vet Emerg Crit Care10:91102, 2000.

Eubig PA, Brady MS, Gwaltney-Brant SM, et al: Acute renal failurein dogs after the ingestion of grapes or raisins: A retrospectiveevaluation of 43 dogs (19922002). J Vet Intern Med19(5):663674, 2005.

Fischer JR, Pantaleo V, Francey T, Cowgill LD: Veterinary

hemodialysis: Advances in management and technology. VetClin North Am Small Anim Pract34(4):935967, 2004.

Kellum JA, Decker JM: Use of dopamine in acute renal failure: Ameta-analysis. Crit Care Med29:15261531, 2001.

Landerville AJ, Seshadri R: Utilization of continuous renalreplacement therapy in a case of feline acute renal failure.J VetEmerg Crit Care14(4):278286, 2004.

Stokes JE, Forrester SD: New and unusual causes of acute renalfailure in dogs and cats. Vet Clin North Am Small Animal Pract34(4):909922, 2004.

Tefft KM: Lily nephrotoxicity in cats. Compend Contin Educ PractVet26(2):149157, 2004.

Vaden SL, Levine J, Breitschwerdt EB: A retrospective case-controlof acute renal failure in 99 dogs. J Vet Intern Med11:5864,1997.

Whittemore JC, Webb CB: Beyond fluid therapy: Treating acuterenal failure. Compend Contin Educ Pract Vet27(4):288298,2005.

Documents

Acute Renal Failure 2006