Bilirubin is one of the major body waste products that require excretion.
70% is derived from the destruction of cells mainly in the spleen and liver, 10% is from bone marrow, and the remainder is from myoglobin breakdown.
Newly formed bilirubin is insoluble in water, and binds to circulating albumin.
This binding allows transport of bilirubin via the blood to the liver, and the now large bilirubin/albumin complex prevents diffusion across cell membranes, and helps to confine bilirubin to the blood vessels.
Binding ability may be reduced by the drugs, Sulphonamides and Salicylate, or in animals suffering acidosis.
Bilirubin separates from albumin prior to entry into the liver cell. Once inside, specific proteins bind the bilirubin; it is then combined with Glucoronic Acid to form bilirubin Monoglucoronide.
The importance of this process is that the bilirubin, previously insoluble in water, has now been transformed into a water-soluble compound, which is essential for its excretion.
Even in the event of considerable liver damage, this part of the system appears to continue to function efficiently.
Normally, the now water-soluble bilirubin is excreted from the liver cells into the bile ducts. However, this excretory system is extremely sensitive to various types of liver damage, and when the liver is under stress, increasing amounts of bilirubin are returned to the Plasma.
On the other hand, in greyhounds with liver damage the Total Plasma Bilirubin may not increase significantly. This is because dogs as a species, easily pass water-soluble bilirubin through the kidneys into the urine, and it is only when both liver and kidney damage occurs, that the plasma levels of bilirubin increase sharply.
The use of tests to measure the quantity of bilirubin in plasma is therefore not an accurate assessment of liver function in dogs.
When total plasma bilirubin exceeds 1.0 mg/dl, one can observe a yellow colour of plasma in a spun micro-haematocrit tube.
Impaired liver function leads to a decreased bile flow and is characterised by increased Serum Bile Acid and Alkaline Phosphates (SAP) levels.
There are drugs that may also cause decreased bile flow and increased serum bile acids; they include Corticosteroids, and long-term treatment with anti-convulsants, such as Dilantin or Phenobarbital.
Other drugs that may cause liver damage in dogs include Mebendazole (Telmintic), and possibly others such as Oxibendazole.
Liver damage may also be caused by Aflatoxins, a mould found on grain type foods.
Greyhounds, as a species, are also extremely sensitive to liver damage from Cholinesterase inhibiting compounds, mainly found in flea killing products.
When treating greyhounds for flea infestations, the product label should be carefully read and products listed as Cholinesterase Inhibiting should be avoided, or at least used strictly as directed.
Ongoing liver damage is often associated with marked increases in Serum Alanine Aminotransferase (ALT), and may include decreased concentrations of Blood Urea Nitrogen (BUN), Albumin and Glucose, with increased Plasma Ammonia, and with Bilirubin appearing in the urine in increased amounts.
A marked reduction of available bile due to liver damage, may also cause low levels of intermittent diarrhoea. This is due to low bile levels reducing fat and carbohydrate digestion, and bacterial action on the partially digested foods producing Lactic Acid and Hydroxyl Fatty Acids that irritate the intestines, and aggravate the diarrhoea by increasing gut secretions of fluid and electrolytes.
To obtain the full picture, any tests for Serum Bilirubin should be accompanied by a urine test for water soluble Bilirubin.
After entering the circulation from the liver urea is filtered through the kidneys, where it plays an important part in the fluid reabsorption ability of the kidneys, and is then excreted in the urine.
Low Blood Urea Nitrogen
Decreased production is most commonly associated with chronic liver damage, or long term consumption of a diet severely restricted in protein.
Kidney disease, diabetes insipidus and some types of nephritis may cause increased excretion. However, increased excretion causing a low BUN is often seen in greyhounds with significant Polyuria.
In some cases this is bought on by Polydipsia (increased thirst) triggered by severe intracellular dehydration.
This in turn may be caused by severe stress, due to a hard run by an unfit greyhound, or one suffering from a bacterial or viral infection.
However, some instances of Polyuria are in fact inflicted by the overuse of diuretic alkalising agents, the indiscriminate use of anti-inflammatory injections in injury treatments, or the use of Glucocorticoid injections, in the belief, that they may improve the greyhound’s performance.
It must be said however, because greyhounds are generally on a high protein diet, normal or slightly lower BUN levels, may not give a true indication of the severity of problems relating to possible kidney disease, resulting in the Polyuria / Polydipsia syndrome, and a varying degree of dehydration.
However, decreased excretion of urea by the kidneys, is the most common cause of an increased BUN, and may be due to partial kidney failure, urinary tract obstruction, and or urinary tract infection.
It is generally believed that urea is relatively non-toxic, but other wastes that accompany increased BUN may cause toxicity and dehydration.
The method most used to treat the symptoms of an increased BUN is intravenous fluid therapy. However a urine specimen obtained prior to treatment, should be submitted for a complete urine analysis, including sediment examination.
Specific treatment of the underlying cause should be started as soon as possible.