Tables 12.1 and 12.2 list the chemical and sedimentary characteristics of normal urine and the changes associated with disease. It is important to make the distinction between physiologic and pathologic changes in color. Normal horse urine varies from pale yellow to almost colorless. The yellow coloration is due to a normal pigment (urochrome) and its intensity can vary in proportion to the specific gravity. Water deprivation results in the excretion of concentrated urine with a higher specific gravity and more intense color. Physiologic dilution of urine can occur with psychogenic polydipsia (q.v.) and with excessive fluid therapy.

Table 12.1

Chemical characteristics of normal equine urine and changes associated with disease

Table 12.2

Sedimentary characteristics of normal equine urine and changes associated with disease

Parameter	Normal content	Disease
Hematuria	None	Hematuria reflects inflammation, trauma, neoplasia or coagulopathy in urinary tract. Trace associated with catheterization
Leukocytes	None	Large numbers associated with inflammation of tract (pyuria)
Transitional	Few	Large numbers reflect inflammation, trauma, neoplasia
Bacteria	None	Moderate to heavy Gram smears/cultures reflect pyelonephritis or cystitis
Crystals	Usually calcium carbonate; occasional triple phosphate; occasional calcium oxalate	Large numbers of triple phosphate indicate infection of tract. Large numbers of calcium oxalate are abnormal, but of uncertain significance
Casts	No cellular casts. Occasional hyaline (mucoprotein) casts	Cellular casts reflect tubular damage in association with protein exudation or leakage

The three most common alterations of urine color from the normal pale yellow color are listed in Box 12.2.

Box 12.2 Common alterations of urine color

Colorless urine

Diseases that result in polydipsia and polyuria (q.v.) frequently result in the production of dilute urine that may be water clear. The principal causes and laboratory features of polydipsia/polyuria are summarized in Table 12.4.

Dark yellow urine

Concentrated urine is produced in the face of dehydration (either a result of pathologic or physiologic relative water loss) or in acute oliguric renal failure (q.v.). The most common cause of oliguria in the horse is dehydration associated with such conditions as diarrhea and colic (q.v.) in which concentrated urine with a deep amber color and high specific gravity may be produced.

Red to brown urine

Urine does not normally contain erythrocytes and it should not have any red discoloration. Samples collected by catheter may have a few erythrocytes; some of these may lyse and so the sample may be red and have an erythrocyte button after centrifugation. Prolonged storage or exposure to air often gives urine a red-brown color (q.v.).

Pathologic red to brown discoloration of urine (pigmenturia) may be a result of one of the following:

1. Hematuria (whole blood in urine)

2. Hemoglobinuria (hemoglobin in urine)

3. Myoglobinuria

4. Certain drugs (e.g. phenothiazine, rifampicin and the diagnostic compound bromsulfophthalein).

Red discoloration is usually due to either hematuria or hemoglobinuria (q.v.). Brown discoloration of urine is generally due to myoglobinuria (q.v.).

Clinical distinction between myoglobinuria and hemoglobinuria can be difficult and usually relies upon electrophoretic or spectrophotometric analysis. Hemoglobin usually derives from plasma and so a comparison to plasma can sometimes be helpful. Myoglobin has a lower molecular weight and lower capacity to bind to protein than hemoglobin and so is usually cleared rapidly by the kidney without any discoloration of the plasma.

Alterations in appearance

Apart from foals, normal horses seldom void water-clear urine. Normal urine is characteristically turbid and mucinous for two reasons:

1. Mucous glands within the ureters and renal pelvis result in the characteristic appearance and texture of equine urine. Mucus secretion is thought to be an evolutionary adaptation to the presence of the rough/irritant calcium carbonate crystals in the urine.

2. On normal diets, urine is often saturated with calcium carbonate, which precipitates spontaneously and gravitates to the floor while urine is held within the bladder. A sample obtained at the onset of urination may be much less turbid than one passed at the end of the stream. Therefore, naturally voided urine and urine collected by catheter frequently appears to vary in its turbidity depending on the part of the bladder being drained at the time. Thick sediment is obtained from the floor while the supernatant is almost clear. Sediment will usually be noted if the container is left undisturbed for a short time.

Normal horse urine will foam on agitation due to the natural protein content.

Routine urinalysis

Routine urinalysis includes the measurement of specific gravity, pH, protein, glucose, bilirubin, urobilinogen and ketones. Usually these are all performed with a single dipstick and results as a rule are clinically reliable. Microscopic examination of urine sediment after centrifugation is a very useful technique but is often complicated by large amounts of calcium carbonate.

Specific gravity

Urine specific gravity (SG) (or, more correctly, its osmolarity) is the only indicator of renal function in the urinalysis. Urinary specific gravity reflects the ability of the kidney to concentrate urine and is therefore a useful indicator of renal function.

1. The specific gravity of normal equine urine varies between 1.020 and 1.050.

2. Dehydration results in a more concentrated urine (SG over 1.035–1.055).

3. Pre-renal azotemia would be indicated by a high SG and elevated urea/creatinine concentrations.

4. The presence of dilute urine (SG of 1.005–1.020) in an azotemic (elevated creatinine and urea concentrations) or dehydrated horse is indicative of renal azotemia (tubular dysfunction).

5. Fluid therapy in a dehydrated pre-renal azotemia case would result in restoration of the normal concentrations of these metabolites. By contrast, a renal azotemia case would simply produce more urine of an equally dilute nature without normalization of the creatinine and urea concentrations. In acute renal failure, fluid therapy would not normally induce urination within 6 h of the initiation of fluid therapy.

On rare occasions, dilute urine may be found in a hydrated, non-azotemic horse as, for example, in diabetes insipidus (q.v.), psychogenic polydipsia (q.v.) or diseases that antagonize the action of antidiuretic hormone.

A 24 h water deprivation test ( Box 12.3, q.v.) may be necessary to assess renal concentrating ability. However, it is imperative that the horse is carefully monitored during the test to avoid dangerous dehydration. Where dehydration is a real or potential hazard, urine-concentrating ability can be measured following the administration of exogenous antidiuretic hormone.

Box 12.3 Water deprivation test

Water deprivation tests are used to identify renal failure and to differentiate psychogenic polydipsia from neurologic (central) and nephrogenic (renal) diabetes insipidus.

These tests must not be performed in horses that are azotemic (q.v.) or show evidence of any dehydration. It is essential therefore that an accurate body weight is taken before embarking on the test, and accurate weighing should be available during the test procedure.

The procedure for a water deprivation test is as follows: