Changes

===Gastro-intestinal Disease===

===Gastro-intestinal Disease===

*'''Oral ulceration''' - This occurs especially at the [[Oral Cavity Overview - Anatomy & Physiology|fauces of the mouth ]]and on the margins of the [[Tongue - Anatomy & Physiology|tongue]]. Halitosis is often a feature of this syndrome as the lesions become secondarily infected with oral bacteria such as ''[[Fusobacterium necrophorum]]''. In severe cases, there may be extensive subepithelial necrosis and sloughing of the tip of the tongue. The lesions are often very painful and contribute to the anorexia often observed in animals with chronic kidney disease. Excessive dental calculus may be evident in animals with chronic kidney disease on oral examination.

*'''Oral ulceration or uraemic stomatitis''' - This occurs especially at the [[Oral Cavity Overview - Anatomy & Physiology|fauces of the mouth ]]and on the margins of the [[Tongue - Anatomy & Physiology|tongue]]. Uraemic vasculitis and thrombosis lead to necrosis and sloughing of the mucosa. There is irritation of the tissues from the ammonia produced by the bacterial degradation of urea. Halitosis is often a feature of this syndrome as the lesions become secondarily infected with oral bacteria such as ''[[Fusobacterium necrophorum]]''. In severe cases, there may be extensive subepithelial necrosis and sloughing of the tip of the tongue. The lesions are often very painful and contribute to the anorexia often observed in animals with chronic kidney disease. Excessive dental calculus may be evident in animals with chronic kidney disease on oral examination.

*'''[[Gastric Ulceration - all species|Gastric ulceration]]''' - This occurs for three main reasons. First, urea crosses lipid membranes freely and enters the gastro-intestinal lumen of azotaemic animals. The urea is degraded to ammonia by bacterial urease and the ammonia irritates the intestinal mucosa. This is compounded by damage to the blood vessels of the gastric submucosa by the fibrinoid necrosis that is a common feature of uraemia.  Elevated serum concentrations of gastrin (which is normally metabolised in the kidney) also lead to excessive production of gastric acid from parietal cells in the stomach. Animals with gastro-duodenal ulceration may show '''anorexia''', '''[[vomiting]]''', '''haematemesis''' and [[Peritonitis - Cats and Dogs|'''peritonitis''']] and '''haemorrhage''' if the ulcers perforate. Hypergastrinaemia may also cause incompetence of the pyloric sphincter of the stomach, permitting reflux of irritant bile into the stomach. Similar processes result in the development of '''uraemic colitis'''.

*'''[[Gastric Ulceration - all species|Gastric ulceration]]''' - This occurs for three main reasons. First, urea crosses lipid membranes freely and enters the gastro-intestinal lumen of azotaemic animals. The urea is degraded to ammonia by bacterial urease and the ammonia irritates the intestinal mucosa. This is compounded by damage to the blood vessels of the gastric submucosa by the fibrinoid necrosis that is a common feature of uraemia.  Elevated serum concentrations of gastrin (which is normally metabolised in the kidney) also lead to excessive production of gastric acid from parietal cells in the stomach. Animals with gastro-duodenal ulceration may show '''anorexia''', '''[[vomiting]]''', '''haematemesis''' and [[Peritonitis - Cats and Dogs|'''peritonitis''']] and '''haemorrhage''' if the ulcers perforate. Hypergastrinaemia may also cause incompetence of the pyloric sphincter of the stomach, permitting reflux of irritant bile into the stomach. Similar processes result in the development of '''uraemic colitis'''.

*'''[[Peritonitis - Cats and Dogs|Uraemic peritonitis]]''' - This is a form of chemical peritonitis that results from inflammation of the small mesothelial blood vessels.

*'''[[Peritonitis - Cats and Dogs|Uraemic peritonitis]]''' - This is a form of chemical peritonitis that results from inflammation of the small mesothelial blood vessels.

The underlying cause of the renal failure should be treated. To alleviate the clinical signs of uraemia, it is particularly important to restrict phosphate by feeding a '''low phosphate diet''' and using '''phosphate-binding drugs''' such as aluminium hydroxide or chitosan. Deficient electroylytes should be supplemented but calcium should only be administered after hyperphosphataemia has been corrected to prevent further mineralisation of soft tissues.

The underlying cause of the renal failure should be treated. To alleviate the clinical signs of uraemia, it is particularly important to restrict phosphate by feeding a '''low phosphate diet''' and using '''phosphate-binding drugs''' such as aluminium hydroxide or chitosan. Deficient electroylytes should be supplemented but calcium should only be administered after hyperphosphataemia has been corrected to prevent further mineralisation of soft tissues.

Various [[Gastroprotective Drugs|gastro-protectant drugs]] can be prescribed to manage the gastro-intestinal signs of uraemia, including sucralfate and the acid secretory inhibitors ranitidine, cimetidine and omeprazole. Appetite stimulants such as mirtazapine can also be administered to anorexic animals to encourage voluntary food intake.

Various [[Gastroprotective Drugs|gastro-protectant drugs]] can be prescribed to manage the gastro-intestinal signs of uraemia, including sucralfate and the acid secretory inhibitors ranitidine, cimetidine and omeprazole. Appetite stimulants such as mirtazapine can also be administered to anorexic animals to encourage voluntary food intake. Oral pain can be controlled by topical application of lidocaine gel or sucralfate paste.

A major advance in the management of uraemia has been the introduction of '''recombinant erythropoietin''' which can be administered to anaemic animals as a series of subcutaneous injections. Some animals may become resistant to its effects over time due to the development of an immune response to the recombinant protein.

A major advance in the management of uraemia has been the introduction of '''recombinant erythropoietin''' which can be administered to anaemic animals as a series of subcutaneous injections. Some animals may become resistant to its effects over time due to the development of an immune response to the recombinant protein.

==Prognosis==

==Prognosis==

Renal failure that is sufficiently severe to cause uraemia is very severe and carries a poor prognosis for recovery. Lost renal function cannot be recovered and the best that can be hoped for is to manage the clinical syndrome as long as the patient maintains an acceptable quality of life.

Renal failure that is sufficiently severe to cause uraemia is very severe and carries a poor prognosis for recovery. Lost renal function cannot be recovered and the best that can be hoped for is to manage the clinical syndrome as long as the patient maintains an acceptable quality of life.

==Literature Search==

==Literature Search==

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal  Medicine (6th edition, volume 2)''' ''Elsevier Saunders''

Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal  Medicine (6th edition, volume 2)''' ''Elsevier Saunders''

[[Category:Oral Cavity - Metabolic Pathology]]

[[Category:Oral Cavity - Metabolic Pathology]]

[[Category:Lungs_-_Pathology]][[Category:Cardiovascular_System_-_Metabolic_Pathology]][[Category:Renal Failure]]

[[Category:Lungs_-_Pathology]][[Category:Cardiovascular_System_-_Metabolic_Pathology]][[Category:Renal Failure]]

[[Category:Expert_Review]]

[[Category:Expert_Review]]