Changes

==Introduction==

==Introduction==

On presentation is it important to establish two things:

Acute Renal Failure is a syndrome caused by the '''acute failure of haemodynamic, filtration and excetory functions in the [[Kidney - Anatomy & Physiology|kidney''']]. This results in the '''accumulation of [[Uraemia|uraemic toxins]]''' and the '''dysregulation of acid-base, fluid and electrolyte balances'''.

 

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

* '''Renal factors''' include acute [[Interstitial Nephritis|interstitial nephritis]]

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

* '''Post-renal factors''' include lower urinary tract obstruction

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'''.

Clinical signs include''' oliguria or anuria, [[Vomiting|vomiting]] and anorexia'''; blood sample analysis shows [[Azotaemia|azotaemia]].

==Aetiology==

==Aetiology==

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

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.  

'''[[Toxicology|Toxic injury]]''' is the most common cause. [[Toxicology|Toxins]] such as '''aminoglycosides, [[Ethylene Glycol Toxicity|ethylene glycol]], [[NSAIDs|NSAIDs]], [[House Plant Toxicity|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 - Anatomy & Physiology|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.  

'''[[Ischaemia|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|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.  

'''Tubulointerstital disease''' resulting in [Inflammation|inflammation]] and [[Oedema|oedema]] can also cause acute renal failure. This is normally precipitated by infections ([[Pyelonephritis|pyelonephritis]] and [[Leptospirosis - Cats and Dogs|leptospirosis]]), [[Autoimmune Diseases|autoimmune reactions]] and [[Allergic Diseases|allergy]].  

==Pathogenesis==

==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)

* A reduction in [[GFR|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

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

==Clinical Signs==

==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.   

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

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

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

'''* Dehydration'''

* '''[[Dehydration|Dehydration]]'''

'''* Lethargy'''

* '''Lethargy'''

'''* Malaise'''

* '''Malaise'''

'''* Vomiting'''

* '''[[Vomiting|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.  

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

==Diagnosis==

==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.  

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:

As mentioned it is important to differentiate ARF from decomensated [[Chronic Renal Failure|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'''

'''(1) History'''

'''(2) Renal'''

'''(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'''.  

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'''. The hallmark of primary renal failure is azotaemia in the presence of poorly concentrated urine.

'''(3) Post-renal'''

'''(3) Post-renal'''

==Treatment==

==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.

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|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|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'''.  

'''Aggressive [[Fluid therapy|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 Effects on Kidneys - Anatomy & Physiology|'''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.

Severe '''metabolic disturbances''' occur secondary to ARF. '''Hyperkalaemia''' is a common occurrence and is also treated with '''fluid therapy''' using a product such as saline. 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.

Additional supportive treatment includes '''anti-emetic drugs''' and [[Gastroprotective Drugs|'''gastro-protectants''']] such as sucralfate and ranitidine. A low protein diet can be fed to reduce the levels of uraemic toxins and an oesophageal tube should be placed in any anorexic animals.  

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

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.  

'''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.   

'''Haemodialysis:''' 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==

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'''.

Prognosis is entirely dependant on whether the animal can be supported whilst the tubules repair. Often intensive care for prolonged peroids (up to eight weeks) is required to achieve this. Generally, animals presenting with '''oliguria''', particularly with a history of toxin ingestion have a '''grave prognosis'''. Renal biopsy may give an indication of the reversibility of the condition and therefore prognosis - it should be considered prior to starting dialysis. If urine production is not restored following treatment, prognosis is very poor and euthanasia may be the only appropriate option.

 

 

 

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