Page 534 - WSAVA2018
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 25-28 September, 2018 | Singapore
Bilirubin is not produced in birds and reptiles; they utilize biliverdin instead. There are no commercial assays for biliverdin. Bilirubin is useful for evaluating cholestasis in small mammals.
Kidney function
Birds: The end-product of protein metabolism in
birds is uric acid. It is produced in the liver, enters the circulation and is then secreted by renal tubules (>90%) or filtered in the glomerulus (<10%). Significant loss of renal tubules will therefore result in elevations of uric acid. Dehydration is less likely to cause hyperuricaemia because glomerular filtration is relatively unimportant.
At first glance it would appear that uric acid offers a sensitive and specific test for renal disease. There are, however, several confounding factors. Firstly, species differences: carnivorous birds have higher normal
uric acid levels than granivorous birds. Secondly, age: juvenile birds may have lower levels than adults. Thirdly, although significant elevations usually indicate renal disease, normal levels do not mean the kidneys are normal: mild increases could indicate early renal disease or dehydration (or both). There must be severe renal damage before uric acid levels begin to rise.
Because of this relative insensitivity of uric acid in detecting renal disease, levels are best interpreted alongside a determination of the bird’s water intake and loss and a physical examination. To distinguish renal disease from dehydration, the patient’s haematocrit, total protein and blood urea nitrogen (BUN) should
be evaluated concurrently. Dehydration can lead to decreased glomerular filtration rates (GFRs), in turn leading to elevated levels of BUN; this same decrease in GFR can lead to elevations of uric acid without primary renal disease being present. It is therefore prudent, in cases of an elevated uric acid level, to rehydrate the patient over 2–3 days before definitively diagnosing renal disease. Persistent hyperuricaemia after fluid therapy, and with haematocrit, total protein and BUN returning to normal, confirms a diagnosis of renal disease.
Creatinine is generally accepted as being of little or no value in evaluating renal function in birds. Phosphorus elevations are usually not seen in birds with renal disease.
Reptiles: Hyperuricaemia in reptiles is commonly associated with high protein diets, a recent meal, dehydration, and gout. It is not commonly observed in reptiles with renal disease. This is because it is excreted in the proximal tubules and so it is usually widespread renal disease that affects blood concentrations. Elevations in urea nitrogen may be associated with pre- renal, renal, or post-renal disease. Hypocalcaemia and hyperphosphataemia are common in reptiles with renal disease, with a Ca:P ratio less than 1.0 been strongly
lar or hepatocellular damage. AST, therefore, must be interpreted alongside CK (released from damaged muscle) to distinguish between the two. In general, an elevated AST with a normal CK indicates hepa- tocellular rupture. However, CK has a much shorter half-life than AST; a single-point muscle injury (e.g. an injection) 4–7 hours before sample collection could duplicate this biochemistry pattern. Although AST
is considered to be the most useful liver enzyme, it cannot be considered in isolation as an indicator of liver disease.
· Glutamate dehydrogenase (GLDH), a mitochondrial enzyme, is the most specific enzyme for the detec- tion of liver disease, but its sensitivity is low. Because it is bound to mitochondria, extensive and severe liver damage is required before elevations are de- tectable.
· Lactate dehydrogenase is not specific to any tissue; its main advantage lies with a half-life shorter than CK. Persistent elevation in the presence of normal CK is strongly suggestive of liver disease.
· Alanine aminotransferase (ALT) and alkaline phos- phatase are not considered useful in detecting liver disease in birds, reptiles and rabbits. ALT in these species is very nonspecific for the liver, and normal levels have been shown in cases with severe liver damage.
Decreased liver function
Decreased liver function can occur with any number of liver diseases, not all of which involve hepatocellular rupture. Chronic cirrhosis, amyloidosis and hepatic lipidosis can all have an adverse effect on liver function without causing any cellular damage. In these cases a ‘liver function test’ is necessary to detect the problem. Bile acids serve this purpose well. Produced in the liver, they are excreted in bile into the small intestine where they act to emulsify fat. Most of the bile acids are then resorbed in the small intestine, enter the portal system and are taken up by the liver to be recycled. Elevated levels occur when there is impairment of the liver’s ability to remove bile acids from the portal circulation.
A two- to fourfold increase in bile acids indicates a significant decrease in liver function. It needs to be noted though that a severely dysfunctional liver (e.g. end-stage cirrhosis) may not be able to produce normal levels of bile acids, leading to low to normal results. Total protein, especially albumin, may also be decreased with decreased liver function.
Cholestasis occurs when the biliary system is partially or totally obstructed. This can be seen with biliary neoplasia, pancreatic disease or diffuse swelling of the entire liver. Gamma glutamyl transferase (GGT) is an enzyme found in the cell membranes of the bile ducts. Elevations can be seen in cholestatic disease (e.g. bile duct carcinoma), but it is considered to be a relatively insensitive test for liver disease in parrots.

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