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Uraemia describes the clinical syndrome caused by [[Azotaemia|azotaemia]], an increase in the blood concentrations of urea and creatinine. The major cause of azotaemia is [[Kidney Renal Failure - Pathology|renal failure]] but it is an insensitive indicator of this disease, only becoming detectable when more than approximately two thirds of the nephrons are no longer functional.
Uraemia describes the clinical syndrome caused by [[Azotaemia|azotaemia]], an increase in the blood concentrations of urea and creatinine. The major cause of azotaemia is [[Kidney Renal Failure - Pathology|renal failure]] but it is an insensitive indicator of this disease, only becoming detectable when more than approximately two thirds of the nephrons are no longer functional.
Uraemia affects causes pathological changes of arteriolar fibrinoid degeneration and this affects multiple organ systems and produces marked clinical signs. It may develop acutely or it may develop gradually in animals with chronic kidney disease.
===Pathophysiology===
Uraemia causes pathological changes of arteriolar fibrinoid degeneration and this affects multiple organ systems and produces marked clinical signs. It may develop acutely or it may develop gradually in animals with chronic kidney disease.
Uraemic toxins - P, CT, PTH.
==Signalment==
==Signalment==
===Clinical Signs===
===Clinical Signs===
[[Image:uraemia.gif|right|thumb|125px|<center>Lesions due to uraemia associated with pyelonephritis and chronic kidney disease<br><small>Copyright Alun Williams 2007 (RVC))</center></small>]]
[[Image:uraemia.gif|right|thumb|125px|<center>Lesions due to uraemia associated with pyelonephritis and chronic kidney disease<br><small>Copyright Alun Williams 2007 (RVC))</center></small>]]
The most common signs of uraemia are:
The most common syndromes encountered in animals with uraemia are:
*'''Oral ulceration''', especially at the [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|fauces]] of the mouth and on the margins of the [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]]. Halitosis is often a feature of this syndrome as the lesions become secondarily infected oral bacteria such as ''[[Fusobacterium necrophorum]]''. On clinical examination, there may also be excessive dental calculus in animals with chronic kidney disease. 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.
*'''Oral ulceration''' - This occurs especially at the [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|fauces]] of the mouth and on the margins of the [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]]. Halitosis is often a feature of this syndrome as the lesions become secondarily infected oral bacteria such as ''[[Fusobacterium necrophorum]]''. On clinical examination, there may also be excessive dental calculus in animals with chronic kidney disease. 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.
*'''Gastric ulceration''' occurs for two 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 the manifestations of uraemia. Animals with gastro-duodenal ulceration may show '''anorexia, vomiting, haematemesis''' and [[Peritonitis - Cats and Dogs|'''peritonitis''']] if the ulcers perforate.
*'''[[Gastric Ulceration - all species|Gastric ulceration]]''' - This occurs for two 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 the manifestations of uraemia. Animals with gastro-duodenal ulceration may show '''anorexia, vomiting, haematemesis''' and [[Peritonitis - Cats and Dogs|'''peritonitis''']] if the ulcers perforate. Similar processes result in the development of '''uraemic colitis'''.
*Damage to the small vessels of the pulmonary vasculature may result in '''pulmonary oedema''' and '''pleural effusion''' with dyspnoea, tachypnoea and coughing.
*'''[[Pulmonary Oedema|Pulmonary oedema]]''' - Damage to the small vessels of the pulmonary vasculature may result in pulmonary oedema and pleural effusion with dyspnoea, tachypnoea and coughing.
*Electrolyte imbalance.
*'''Electrolyte imbalances''' - The failure to excrete phosphate through the damaged kidneys results in hyperphosphataemia. This complexes with calcium and also prevents the activation of vitamin D (dihydroxycholecalciferol), resulting in hypocalcaemia. This hypocalcaemia directly stimulates the production of parathyroid hormone (PTH) to try to maintain normal blood calcium levels and, in ~10% dogs with renal failure, hypercalaemia may develop due to an alteration in the set-point at which PTH is secreted. In the remaining 90%, calcium is mobilised from bone causing '''secondary renal hyperparathyroidism''' with pathological fractures of various bones.
*Uraemic peritonitis and colitis.
*'''[[Peritonitis - Dogs and Cats|Uraemic peritonitis]]''' - This is a form of chemical [[peritonitis]] that results from inflammation of the small mesothelial blood vessels.
*Atrial rupture.
*'''Atrial rupture''' - Mineralisation of the atria reduces their normal compliance and renders them susceptible to rupture. The resultant haemopericardium is often fatal as it causes acute cardiac tamponade.
*Mineralisation.
*'''Metastatic mineralisation''' - The presence of excessive blood concentrations of phosphate leads to metastatic calcification in multiple tissues, particularly the rugae of the gastric mucosa, the pulmonary parenchyma, the heart ...
*Thrombocytopathia.
*'''Thrombocytopathia'''.
*Arrhthymias.
*'''[[Arrhthymias Overview|Arrhthymias]]'''.
*Neurological disease.
*'''Neurological disease''' - The presence of extremely high concentrations of urea and creatinine may induce '''uraemic seizures''' and this is usually a terminal event.
*'''Anaemia''' - The diseased kidenys produce less erythropoietin than normal but the uraemic toxins also decrease the lifespan of existing red blood cells. Erythrocytes may also be damaged as they pass along inflamed vessel walls, a form of microangiopathic haemolysis.
===Laboratory Tests===
===Laboratory Tests===
Serum biochemistry will show elevated levels of [[Urea|urea]] and [[Creatinine|creatinine]]. Animals with acute renal failure may by '''hyperkalaemic''' and '''hyperphosphataemic''' but cats with chronic renal failure are often '''hypokalaemic''' and '''hyponatraemic'''.
In cases of chronic renal failure, there may be a '''normocytic, normochromic, non-regenerative anaemia'''.
===Other Tests===
===Other Tests===
Examination of a urine sample may show signs consistent with renal failure. Animals with acute renal failure may be anuric and those with chronic renal failure may be polyuric but in both cases, the urine will be isosthenuric (with a specific gravity of 1.008-1.012).
===Diagnostic Imaging===
===Diagnostic Imaging===
Imaging may show the presence of metastatic calcification in multiple organs, including...
===Other Tests===
Uraemic carcases?
==Treatment==
==Treatment==
The underlying cause of the renal failure should be treated. To alleviate the clinial 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.
==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.
==References==
==References==