Acute Renal Failure

Introduction

Acute renal failure is rapidly progressive but may be reversible. It can result from pre-renal, intra-renal or post-renal factors. *Prerenal factors include ischaemia and reduced renal perfusion *Renal factors include acute interstitial nephritis *Postrenal factors include lower urinary tract obstruction Clinical signs include oliguria or anuria, vomiting and anorexia; blood sample analysis shows azotaemia.

On presentation is it important to establish two things:

(1) Whether the renal failure is acute or chronic as they present in a very similar manner but have different treatment protocols and prognoses.

(2) Whether the renal failure is pre-renal, renal or post-renal

Acute Renal Failure is a syndrome caused by the acute failure of haemodynamic, filtration and excetory functions in the kidney. This results in the accumulation of uraemic toxins and the dysregulation of acid-base, fluid and electrolyte balances.

Aetiology

This section only covers the intrinsic causes or ARF, as pre- and post-renal failure are very different disease processes.

Toxic injury is the most common cause. Toxins such as aminoglycosides, ethylene glycol, NSAIDs, easter lillies and ACE-inhibitors can all cause renal failure. Some toxic agents act directly on tubular cells, some act on the haemodynamics of the kidney, whilst others cause damage by precipitating within the tubules.

Ischaemic injury is also common, especially following hospitalisation. It is therefore essential to monitor the fluid therapy requirements of hospital patients, especially peri- and post-operatively to prevent pre-renal azotaemia and subsequent ischaemia.

Tubulointerstital disease resulting in inflammation and oedema can also cause acute renal failure. This is normally precipitated by infections (pyelonephritis and leptospirosis), autoimmune reactions and allergy.

Pathogenesis

• A reduction in GFR is caused by the decreased in surface area or conductivity of glomerular capillaries (resulting in a drop in the ultra-filtration coefficient)

• Epithelial cells and debris obstruct the tubules. Toxin precipitates may contribute to this

• Tubular fluid leaks out of the tubules and across the epithelium, back into the interstitium - causing a drop in GFR

• Ischaemic injury to the peripheral medulla occurs due to intra-renal vasoconstriction

Clinical Signs

The most significant information can be gleaned from the history. It is important to ask the owners about toxin ingestion and urine production.

Clinical exams normally reveals fairly non-specific signs such as:

* Dehydration

* Lethargy

* Malaise

* Vomiting

There may also be evidence of swollen or painful kidneys abdominal palpation, an increased or decreased heart rate, hypothermia and oral ulceration or signs of a concurrent disease.

Diagnosis

The most suggestive sign of severe acute renal failure is oliguria or anuria. It does not occur in all cases so should not be completely relied on for diagnosis.

As mentioned it is important to differentiate ARF from decomensated CRF, as ARF is potentially reversible with aggressive therapy. The only diagnostic test that can achieve this is biopsy, but due to the high level of risk involved in an already sick animal this is normally not performed. Instead the following factors can be used by the clinician to guide diagnosis:

(1) History

With ARF there may be a history of ingestion of or access to toxins/nephrotoxic drugs, and oliguria. Cats with CRF normally have a history of chronic weight loss, anorexia and PU/PD.

(2) Clinical Exam

ARF cats tend to have a good body condition score, and healthy skin and coat. CRF cases have a poor body condition score and a dull/scruffy coat.

(3) Renal Parameters - palpation, ultrasound, radiography

The kidneys in ARF cats are normal sized or enlarged, and normally painful. In CRF, the kidneys are shrunken, firm and non-painful

(4) Other

The presence of secondary renal hyperparathyroidism and non regenerative anaemia is suggestive of CRF

Secondly the type of azotaemia must be identified:

(1) Pre-renal

Caused by severe dehydration, shock or any other pathology that results in poor renal perfusion. In these cases USG is >1.035 in the cat and >1.030 in the dog before fluid therapy. There should be no evidence of inflammation and urine sodium concentrations are low. Diagnosis is confirmed by a rapid and dramatic response to fluid therapy.

(2) Renal

This is caused by a direct insult to the kidney, with intrinsic damage. In these cases azotaemia is present, and urine specific gravity is between 1.007 and 1.025. There may be evident of inflammation in the urine sediment and a high sodium content. There is only a minimal response to fluid therapy.

(3) Post-renal

Post-renal failure is caused by an obstruction or rupture with in the urinary system. This is normally identifiable following a thorough history and physical exam.

Treatment

The aim of treatment is to support the patient whilst the tubules repair. If the ingestion of a specific toxin is known then an antidote may be given if available (for example ethanol in ethylene glycol toxicity). More commonly, by the time of presentation the damage to the kidneys has already occurred and it is no longer appropriate to administer the antidote. If any other underlying cause has been identified (such as pyelonephritis), this should be treated appropriately.

Aggressive fluid therapy is the mainstay of treatment in ARF cases. A mild level of volume overload is ideal as it promotes urine production, however as animals are often oliguric, care should be taken not to overload the body with too much fluid. In addition diuretics such frusemide and mannitol can be administered to stimulate urine production. A closed collection system should be used to monitor urine output.

Severe metabolic disturbances occur secondary to ARF. Hyperkalaemia is a common occurrence and is also treated with fluid therapy. If it is severe and compromising the cardiac function of the animal then calcium gluconate can be administered to stabilise the heart (whilst levels are reduced by fluid therapy). Metabolic acidosis also occurs, and again can be treated with fluid therapy. A fluid such as Hartmanns which contains bicarbonate should be used. If this is insufficient to resolve the acidosis then bicarbonate can be administered directly.

Additional supportive treatment includes anti-emetic drugs and gastro-protectants such as sucralfate and ranitidine. A low protein diet can be fed to reduce the levels of uraemic toxins.

It this treatment is not sufficient to maintain the animal then a method of dialysis may be considered.

Peritoneal Dialysis: This technique uses the omentum within the peritoneum as a filter to remove uraemic toxins. It is used in specialist referral centres when it is considered likely that the cat may recover from ARF. The technique is labour intensive but well tolerated by the animal.

Blood Dialysis: This is rarely performed due to the high cost of equipment and ethical questions surrounding longterm treatment. It is only available at a limited number of specialist hospitals.

Prognosis

Prognosis is entirely dependant on whether the animal can be supported whilst the tubules repair. Often intensive care is required to achieve this. Generally, animals presenting with oliguria, particularly with a history of toxin ingestion have a grave prognosis.

Acute Renal Failure Learning Resources
Flashcards Test your knowledge using flashcard type questions	Feline Medicine Q&A 23

Acute Renal Failure Learning Resources
Flashcards Test your knowledge using flashcard type questions	Feline Medicine Q&A 24