Acute Renal Failure: clinical syndrome characterised by the sudden onset of haemodynamics, filtration and excretory failure of the kidneys and the subsequent accumulation of metabolic (uraemic) toxins and dysregulation of fluid, electrolyte and acid-base balance.
Acute Kidney Injury: this term may be preferred in some instances as it indicated that an abrupt decline in kidney function has occurred, although the patient does not have to develop azotaemia.
In human medicine, AKI is recognised to occur when any of the following conditions are met:
An abrupt (within 48 hours) reduction in kidney function
Absolute increase in creatinine of > 25 µmol/l,
or a percentage increase of 50%,
or a reduction in urine output.
In contrast to CKD, ARF is potentially reversible if diagnosed early after its onset and the animal can be supported while the renal injury is repaired. Delay in implementing therapy may result in irreversible renal damage and death of the patient.
In many instances there are no historical or physical examination findings that specifically indicate that ARF is present. Occasionally animals will be presented for known toxin ingestion, or it will be noticed that the animal is anuric or polyuric. More often, the animal is simply unwell, lethargic or vomiting and azotaemia is detected on routine blood work.
Differentiation Between Prerenal, Postrenal and Intrinsic Renal Failure
Postrenal failure (e.g., rupture of the bladder, urethral obstruction) can usually be defined by obtaining a good history and undertaking a careful physical examination. Prerenal causes of azotaemia include severe dehydration and shock, or any other condition that results in poor renal perfusion. Laboratory differentiation between prerenal and primary intrinsic renal failure requires samples of urine to be obtained prior to fluid therapy. No plasma biochemical parameters can be used to make the distinction. Some features that can be used to distinguish between prerenal and intrinsic renal failure are given in the table below.
Urine specific gravity
> 1.035 (cat) > 1.030 (dog)
No evidence of inflammation
Evidence of inflammation (if acute)
Urine sodium concentration
< 10 mmol/l
> 20 mmol/l
Response to fluid therapy
These criteria are an oversimplification, and there are some situations where prerenal azotaemia can occur in an animal unable to adequately concentrate its urine. Examples of these include animals receiving fluids prior to obtaining urine, taking diuretics or glucocorticoids, or suffering from Addison's disease and/or exhibiting hypercalcaemia. In these instances, the cause of the azotaemia is renal, but it is a functional renal failure rather than an intrinsic (structural or primary) renal problem that is causing the azotaemia. This distinction is not academic; some causes of functional renal failure can be treated, and the prognosis may be much better than for dogs and cats with intrinsic renal disease.
Differentiation Between ARF and CKD
This is an important distinction to make at the start of managing a uraemic crisis, as the prognosis in CKD, if it has reached an advanced stage, is poor unless an important factor in causing its acute decompensation can be identified and treated aggressively.
A summary of important points includes:
A history of chronic weight loss, diminishing appetite and polyuria/polydipsia would suggest CKD, whereas a history of access to nephrotoxins or treatment with nephrotoxic drugs would suggest ARF.
Physical examination findings of poor body condition and poor quality hair coat would suggest CKD, whereas findings of good body condition and hair coat would suggest ARF.
Renal size measured by palpation, radiography or ultrasonography is a useful parameter. This typically reveals small fibrotic kidneys in cases of chronic disease and swollen painful kidneys in ARF which are normal sized or slightly enlarged. There are, however, a number of chronic diseases yielding normal to large-sized kidneys.
The presence of secondary renal hyperparathyroidism (not just hyperphosphataemia) with resorption of bone, particularly around the teeth, would be good evidence of CKD. It is rare for 'rubber jaw' to be clinically apparent.
None of the biochemical laboratory tests can be used to differentiate acute from chronic disease.
A nonregenerative anaemia is typical of CKD.
Perhaps the ultimate diagnostic test and prognostic indicator is renal biopsy, which would differentiate acute from chronic decompensated renal disease and may provide an aetiological diagnosis. However, renal biopsy is an invasive procedure that is not without risk. If the clinical course of the disease and the response to therapy cast doubt on the reversibility of the renal lesions, renal biopsy should be considered.
The best strategy for managing ARF is to prevent it occurring in the first place. While it is not possible to prevent dogs and cats from ingesting toxins, developing heat stroke, etc., many cases of ARF are acquired while the animal is in the hospital. Prevention of ARF requires the anticipation of clinical settings and particular patients at high risk for development of hospital-acquired ARF.
Patients at particular risk include those with:
Systemic disease/multiple organ failure
Drug therapy (NSAIDs, aminoglycosides, cisplatin, amphotericin, ACE-inhibitors)
The most consistent renal protective effect is provided by the correction of fluid deficits and mild volume expansion.
1. Prevent continued toxin exposure. Induction of vomiting/gastric lavage/activated charcoal may be appropriate in some cases of recent exposure. If these methods are used it is important to maintain euvolaemia.
2. Give specific antidotes for toxins if these are available.
3. Treat primary diseases.
4. Correct fluid deficits and dehydration. This requires very close monitoring of animals that are potentially oliguric or anuric to prevent the development of hypervolaemia. This requires very careful monitoring including serial measurements of body weight, urine output, central venous pressure, PCV/TP and repeated physical examination.
5. Rectify potassium balance and acid-base disturbances.
6. Conversion from an oliguric (low output of urine) to a polyuric state (if required). It is very important to realise that increasing urine flow does not equate to an increase in GFR. In fact, if renal replacement therapies, such as dialysis, were available for our patients, it is unlikely that we would use any of these treatments.
a. Mannitol (0.25–1.0 g/kg as a slow IV bolus over 10–20 minutes), proposed to increase renal blood flow, decrease cellular swelling, dispense tubular debris and scavenge free radicals. Must not be used if the patient is overhydrated or in congestive heart failure.
b. Furosemide (boluses of 2–4 mg/kg or CRI of 0.5–1.0 mg/kg/h) either alone or in combination with mannitol or dopamine to promote formation of urine and facilitate management of overhydration and hyperkalemia. If improperly monitored, diuretics may deplete circulating volume, precipitating a prerenal insult on established renal injury.
c. Dopamine (1–3 µg/kg/min), a catecholamine suggested to cause renal vasodilation at these doses. Its use is very controversial and most criticalists do not currently recommend its use. Higher doses cause undesired vasoconstriction, tachycardia and arrhythmias. Dopamine and furosemide may act synergistically to increase urine production. Should not be used in cats.
d. Diltiazem (1–5 µg/kg/min) has been suggested as an alternative treatment in dogs with ARF. The rationale is that it will cause preglomerular arteriolar dilatation.
7. Control vomiting and address nutritional requirements.
8. Renal replacement therapy (hemodialysis or peritoneal dialysis).
It is important to recognise that in most instances we are not able to 'treat' ARF directly. All we are able to do is try to maintain the animal while the kidneys try to repair themselves.
1. Sigrist NE. Use of dopamine in acute renal failure. Journal of Veterinary Emergency and Critical Care. 2007;17:117–126.
2. Mathews KA, Monteith G. Evaluation of adding diltiazem therapy to standard treatment of acute renal failure caused by leptospirosis: 18 dogs (1998–2001). Journal of Veterinary Emergency and Critical Care. 2007;17:149–158.