The urinary system

Chapter 12

The urinary system

Chapter contents


The upper urinary tract comprises the kidney and the ureters. The kidneys are responsible for the fine-tuning of the water and electrolyte balances, and the amount of water ingested or produced metabolically can have a significant effect on urine production. The ureters conduct the urine to the bladder in a pulsatile fashion with muscular contractions delivering accumulated urine from the renal pelvis to the bladder up to 6–10 times per minute.

The bladder and urethra make up the lower urinary tract. The bladder stores urine and the urethra conducts it out of the body.

Normal horses produce between 5 and 15 mL urine per kg body weight per day but this varies with food type and the extent of loss of water from the gut, the respiratory tract and skin. Even during extreme dehydration urine will be produced at approximately 2.5 mL/kg/day.

Renal disease affects the whole body but the common clinical features of equine urinary tract disease are non-specific. From a clinical perspective urinary tract disease is manifest by:

Related non-specific systemic signs include anorexia, depression, ventral edema, oral ulceration and colic.

Normal horses pass urine freely after posturing appropriately, and the ability to posture correctly has an important role in the ability and willingness of the horse to urinate. If the horse cannot (for pain or physical reasons) posture correctly an impression of urinary tract disease may be displayed.

For the most part, weight loss is an indicator of renal disease while bladder and urethral problems are associated with abnormal urination.


The normal equine bladder can accommodate 4–4.5L of urine. Horses usually urinate four to six times daily and, depending on size, will produce between 3 and 15L of urine. The volume and composition of normal urine changes frequently in response to external influences such as water consumption, dietary composition, ambient temperature, exercise and natural diurnal variations.

Bladder function is governed by sympathetic, parasympathetic and somatic nerves. Throughout filling, afferent (sensory) neurons induce increased sympathetic activity, which inhibits detrusor contraction. Passive outflow of urine from the urinary bladder is prevented by muscular tone in the neck of the bladder and the proximal urethra. Bladder distension triggers micturition by coordinated contraction of the bladder detrusor muscle, which generates intravascular (bladder) pressure, and simultaneous relaxation of the bladder and urethral “sphincters”. Higher centers in the motor cortex, midbrain and medulla can both inhibit and facilitate contraction by over-riding the automatic local functions. In this way urination can be consciously delayed.

The diagnosis of urinary tract disease presents a clinical challenge because many of the most serious signs are subtle. As a result, cases are often presented with advanced disease. Differentiating between pre-renal (decreased renal perfusion), renal (renal damage or compromise) and post-renal (obstructive lower urinary tract disease or uroperitoneum) disease is a cornerstone of renal medicine.


Urinary tract disease presents with a variety of clinical signs that relate to the etiology, the extent of renal compromise and the organs that are affected secondarily. Thus, difficulty with or pain during urination can be a sign of an obstructive or inflammatory condition in the lower urinary tract (usually the bladder or the urethra). Polydipsia or oliguric renal failure results in little pain but there are significant alterations in urine production. The volume and quality of urine produced may be the only outward evidence of severe renal disease. Advanced renal failure with azotemia and uremia has profound effects on almost all the body organs. Additionally, central nervous signs, anemia, weight loss, oral and intestinal ulceration, are all possible.

Obvious difficulty with urination (dysuria) or variations in the color and character of urine are often the signs that owners will notice. In contrast, because the early signs of renal or lower urinary tract compromise are often subtle, owners may not notice any problem until the condition is advanced.

A thorough clinical investigation is essential in every case of suspected urinary tract disease; the urinary tract should not be overlooked when investigating a variety of other apparently unrelated clinical signs such as colic and weight loss (q.v.) and must be carefully assessed in every case of suspected urinary tract disease.

The clinical investigation of urinary tract disease relies heavily on urinalysis and biochemical tests, but subtle (or sometimes more obvious) clinical indicators of disease do exist; the role of the clinician is to identify these and assess their combined importance.

The limitations to clinical examination mean that there is an increased reliance upon other diagnostic aids. Urinary tract endoscopy (including ureteroscopy) and percutaneous and transrectal ultrasonography, in particular, have significantly improved the prospects of a definitive diagnosis. In adult horses, useful physical examination is limited to rectal palpation. The procedure is indicated in all cases of suspected urinary tract disease.


The value of rectal palpation for urinary tract disease depends upon the relative sizes of the operator and the horse and operator experience. In the case of foals, rectal examination is not feasible but in some cases the bladder can be palpated abdominally.

It is usually only possible to assess the size, texture and outline of the caudal pole of the left kidney. The right kidney is best regarded as non-palpable. The size, wall thickness and texture of the urinary bladder can be appreciated and sometimes abnormal content or masses can be felt. The texture of the bladder can be a major diagnostic aid. In some cases repeated examinations will need to be made to establish variations in function during the normal cycle of filling and emptying.

Unless they are enlarged or inflamed (or both) the ureters are not usually identifiable. It may be more rewarding to palpate the distal regions of the ureters of a mare per vaginam. If the ureters can be felt easily, they can be taken to be abnormal. In any case, the trigone of the bladder should always be palpated. In mares it may be possible to palpate the vesicoureteral opening directly via the urethra and then it may be feasible to pass a catheter directly into the ureters.


Cystoscopy is a simple procedure in mares, although it is sometimes difficult to maintain insufflation. Male horses require a longer thinner endoscope (<1 cm diameter, >1 m long). Videoendoscopy is very helpful but suction apparatus is essential.

Saline distension of the bladder during endoscopy in both male and female is recommended because, in contrast with air insufflation, there is little or no iatrogenic superficial inflammation. Urine samples should be taken before insufflation or distension to avoid artifactual results.

Ureteroscopy and visualization of the renal pelvis is possible with a suitably sized instrument. It is then possible to sample urine from each kidney independently. This procedure does, however, carry risks of introducing infection from the lower tract.

Endoscopic biopsy of pathologic lesions is possible but the biopsy instruments are usually too small to obtain meaningful specimens.


Renal biopsy is a useful technique and can provide a definitive diagnosis in many cases, especially in diffuse renal disease. However, the procedure carries significant risks including perirenal hematoma and heavy (possibly fatal) hemorrhage, and is only justified if histopathology is likely to have a significant influence on subsequent therapy. Biopsy specimens examined by light microscopy may appear normal despite clinicopathologic evidence of severe dysfunction and so the value of biopsy is not always worth the risks. Experience is invaluable in minimizing the problems and meticulous procedural technique will limit the number of biopsies required and the associated risks.

Ultrasound guidance is essential and enables a specific site to be biopsied safely. Biopsy of the right kidney via the 17th intercostal space is the preferred procedure and is diagnostically useful provided that a diffuse bilateral condition such as chronic active glomerulonephritis is present. The left kidney is less simple and usually can only be sampled by crossing the spleen first. In some cases the biopsy instrument can be guided past the spleen directly into the left kidney.

Automatic or spring-loaded biopsy instruments and adequate restraint (stocks and sedation) are important considerations. The clinician must ensure familiarity with the specific biopsy instruments to be used.

The procedure is best performed under standing sedation using a suitable chute or stocks and an IV combination of an α2-adrenoreceptor agonist drug (such as romifidine 0.07 mg/kg, or detomidine 0.03 mg/kg) with an opioid such as butorphanol (0.05–0.1 mg/kg). The procedure should be performed after aseptic preparation of the skin at the chosen site and immediately prior to biopsy an ultrasound check should be made. In some circumstances it may be possible to guide the biopsy instrument using simultaneous ultrasound examination. In all cases biopsy must avoid the renal hilus. Preferred sites are at the caudal pole of the kidney although the location of focal lesions will have a significant influence on the technique and direction of biopsy.

Two biopsies should be obtained: one fixed in 10% formalin solution for histopathology and a frozen one for bacteriology, immunofluorescence testing and electron microscopy.


Radiography has limited diagnostic value in examining the urinary system of adult horses, even when contrast studies are used, but in foals the procedure can be helpful. Diagnosis of bladder and ureteral problems in foals can sometimes be confirmed directly but single or double contrast studies can give added information. Inflation of the foal’s bladder with 200–250 mL air provides a negative contrast that will possibly identify some pathologic changes in the bladder wall (such as defects in the wall). Positive contrast materials based on iodine (such as iohexol) can be infused directly into the bladder via a urethral catheter but can also be infused IV to provide a positive contrast excretory urogram. Positive contrast IV excretory pyelography is performed by injecting an appropriate volume (1 mL/kg iohexol) IV. All these techniques are usually performed in the standing foal.

IV pyelography/excretory urograms can be performed in adult horses and are used mainly to identify ectopic ureters. Suitable contrast medium (e.g. iohexol) is administered by slow IV injection (at a rate of 1 mL/kg body weight) via a jugular catheter. The first radiographs are taken at 3 min and then sequential views are taken at 2 min intervals thereafter for 6–10 min. By this stage the contrast should be clearly visible in the renal pelvis and passing down the ureters. An ectopic ureter will be seen to discharge into an abnormal site (e.g. the anterior vagina) whereas in the normal ureter(s) the contrast will accumulate in the bladder and be clearly visible. The technique has limitations of size and facilities to take diagnostic lateral radiographs. Combinations of positive and negative contrast can be helpful also but these can be logistically more difficult.


Soft tissue phase gamma scintigraphy and urinary clearance of a radionuclide provide a new and exciting diagnostic mode in some specialized centers. The IV administration of technetium 99 m results in rapid delivery of the radiopharmaceutical into the urine, and imaging with a high-resolution gamma camera can identify the individual kidneys and ureters within minutes of injection. Delivery to the bladder (or ectopic location of a ureter) can be detected. Similarly a poorly perfused kidney may have little gamma activity when compared to the contralateral normal kidney or when compared with normal kidneys in the event of a bilateral vascular problem. Tumors and sites of inflammation may be detected by prolonged retention of radionuclide in an affected kidney. During orthopedic scintigraphy the delivery of the radionuclide to the bladder can be a significant complication.


The hemogram provides non-specific information in cases of renal failure. Increases in hematocrit indicate dehydration, and in chronic disease a non-regenerative anemia is expected. Leukocytosis may accompany inflammation of the upper urinary tract and an elevated plasma fibrinogen concentration is usually indicative of septic inflammation.

Serum creatinine is widely used as an indicator of renal disease while blood urea is somewhat less useful. In combination these two metabolites can provide significant information but the concentrations of any blood metabolite must be considered along with the hydration status of the patient.

Creatinine is a metabolite derived from muscle function that is selectively excreted by the renal tubules after being freely filtered into the urine and is then concentrated in the urine. Dietary protein has no material effect on the production of creatinine. Creatinine is estimated directly from serum or urine and the ratio of blood creatinine to urinary creatinine is usually taken as a measure of renal perfusion or more specifically glomerular filtration rate (GFR, q.v.).

Urea excretion is completely passive and the high urinary concentration is achieved directly as a result of medullary hypertonicity in the loop of Henle. Therefore, although high dietary protein results in a corresponding increase in urea excretion, low protein diets do not reduce the “work” of the kidney. Urea is measured from serum or plasma and is a routine laboratory procedure.

Azotemia is a laboratory-derived term used when there are increased blood concentrations of urea and creatinine (and other non-protein nitrogen) in blood. The term uremia (uremic syndrome) is used to describe the widespread effects of high concentrations of urea (azotemia) on body tissues. There is a poor correlation between the severity of uremia and the laboratory-derived concentrations of urea and creatinine. The extent of azotemia is usually highest with renal and post-renal azotemia but the best approach is probably achieved by comparing the blood and urinary creatinine and urea concentrations:

Repeat estimation of urea and creatinine at 24–72 h intervals over the initial period of treatment is probably the most useful practical indicator of the nature and prognosis of the condition.

Dietary intake and gastrointestinal function, hydration, acid-base balance, GFR, urinary volumes and the type of renal lesion govern plasma electrolyte concentrations. It is seldom possible to define a state that is invariably consistent with renal failure.

Since the kidneys are the main sites of potassium excretion, anuria or oliguria is likely to be associated with hyperkalemia, but progressive tubular damage may then lead to hypokalemia.

Oliguria and anuria may cause increased plasma concentrations of sodium and chloride, but progressive tubular damage will be associated with their loss and plasma concentrations may reflect this. If tubular damage is associated with polyuria, then plasma concentrations of sodium and chloride may be within reference ranges (q.v.) as a result of dehydration. Renal dysfunction may be associated with hypercalcemia and hypophosphatemia.

Renal failure also causes a shift in the acid-base balance. Failure of alkali reserve regulation by tubular cells leads to a state of metabolic acidosis (q.v.); this may cause an increase in respiratory rate and depth (Kussmaul’s respiratory pattern).

Indirect biochemical indicators of renal disease include anemia (q.v.), hypoalbuminemia and hypercalcemia.

Anemia is a common secondary sign of advanced renal failure, arising from the combination of failure of renal erythropoietin production (reduced production of erythrocytes) and direct bone marrow suppression arising from uremia.

Hypoalbuminemia arises from protein loss in the urine.

Pathologic failure of the normally dominant calcium excretion of the equine kidney results in a clear urine (free of the normal calcium carbonate crystals) with calcium retention. Calcium excretion in horses is the dominant feature but the extent depends largely on dietary calcium content. Complete absence of calcium carbonate crystals in normal alkaline urine can therefore be physiologic or pathologic. Hypercalcemia can be a helpful diagnostic feature of advanced renal failure, but there are other conditions, including paraneoplastic pseudoparathyroidism (q.v.), that result in a similar finding.


Visual inspection

Urine should be visually inspected as soon as it is collected; normal horse urine may change color to red or brown after standing due to the presence of an oxidizing agent known as pyrocatechin. Owners observing discolored urine collected on concrete floors or in snow sometimes mistake this as abnormal.

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.

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

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

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:

Interpretation of the test can be summarized as follows:

It should be noted that renal medullary washout is due to excessive drinking in the absence of pathology and follows the loss of osmotic gradient within the renal tubules. In this case it is possibly better to perform a partial water deprivation test. The partial water deprivation test is performed by restricting water intake to 40–45 mL/kg/day for several days; water should be offered in small volumes frequently through the day. This will usually restore the gradient, the urine SG will rise to >1.025 and the associated polydipsia will usually resolve. An increase in SG >1.025 suggests psychogenic polydipsia (q.v.) while failure to concentrate >1.025 suggests diabetes insipidus (q.v.).


Horse urine is usually alkaline (pH 7.0–9.0). Attempts to acidify urine (to assist dissolution of calculi or treat bacterial infections of the lower urinary tract) traditionally relied upon dietary administration of ammonium chloride or sodium acid phosphate (sodium dihydrogen phosphate). Neither method is well tolerated and neither is effective.

Acidic urine can be established by alteration of the acid-base balance of the diet (dietary cationanion balance/DCAB). It is calculated using the equation:


Acidification results because of the ion exchange that takes place in the kidney and gastrointestinal tract. A diet with a high DCAB value (300+) increases body pH, while one with a low DCAB (<100) reduces body pH. A low DCAB diet is generally high in Cl ions. High Cl causes a release of bicarbonate ions into the gastrointestinal tract and urine. This leads to a drop in body pH. On the other hand, a high DCAB diet is high in Na+ and particular K+ ions. High cation intakes increase intestinal loss of H+ and increase absorption of Na+ and K+ leading to an increase in body pH. Low dietary DCAB, i.e. diets that are anionic or acidic, cause a metabolic acidosis (q.v.), which in turn reduces the pH of blood and urine. If the horse is producing acidic urine, the normal sediment of calcium carbonate crystals may not form. Low DCAB rations also increase urinary mineral loss, particularly calcium, and so the urine could become cloudier, if the urine pH did not become acidic.


Normal horse urine contains neither blood nor hemoglobin. Erythrocytes, free hemoglobin and myoglobin are the most common abnormal pigments in horse urine and they can often be detected visually. Ortho-toluidine test strips can identify invisible amounts of blood (microhematuria) or hemoglobin and can also differentiate between free hemoglobin (hemoglobinuria) and intact erythrocytes (hematuria) (q.v.).

Red cells in the urine (hematuria) usually derive from renal or post-renal hemorrhage; the latter are more common but the former are usually more profuse (q.v.). The red color will fall to the bottom of the sample when centrifuged or allowed to sediment if hemorrhage is present.

Free hemoglobin (hemoglobinuria) usually derives from intravascular hemolysis. Centrifugation of a truly hemoglobinuric urine specimen will result in no detectable “button” of red cells at the bottom of the tube and a uniform redness to the spun sample.

Combined hematuria and hemoglobinuria may be found on some occasions, such as if erythrocytes lyse in hyposthenuric urine, and so both intact cells and free hemoglobin may be detected.

It is important to realize that erythrocytes may hemolyze if the urine sample is either stood for any length of time or if the sample is agitated roughly. Careful collection, prompt cooling of the sample and timely analysis are, therefore, recommended. Collection of free-flow samples during micturition can give a misleading result and so it is sometimes helpful to obtain the whole urine production or sequential samples so that analysis can provide useful information. Catheterization of the bladder of mares or geldings is practical but again the sample so obtained may be misleading. In general it is wise to collect several samples unless a diagnosis can be established definitively from a single one.

A positive “hemoglobin” test may also arise if myoglobin is present, but it cannot identify myoglobin specifically. Differentiation between myoglobin and hemoglobin can be made using spectrophotometric methods and/or the ammonium sulfate precipitation test (Blondheim test *, Box 12.4) (q.v.). Unfortunately this test has largely been ignored but it is a simple and practical way of separating out the two major causes of pigmenturia.

The Blondheim test is applicable to freshly voided urine or to properly preserved urine. Urine can be preserved for the test by adjusting the pH to 7.0–7.5 (this actually approximates to normal urine but not necessarily to urine from horses with acidosis) and then refrigerated at 4°C. Urine preserved in this way can be tested for up to 2 mo or more despite a moderate degree of bacterial contamination.

Urine sediment

Microscopic examination of the centrifuged sediment in the laboratory is rewarding. Normal sediment usually has a large amount of calcium carbonate crystals. Abnormal crystals include calcium oxalate and calcium phosphate. Urine sediment from normal horses may occasionally contain hyaline casts that appear as slightly refractile tubular structures, especially if the horse is undertaking strenuous work, but granular/protein, erythrocytic and fatty tubular casts are abnormal. These are denser and have a better defined form than the rather amorphous hyaline casts. A small number of leukocytes and bacteria may be observed in normal horses, especially in naturally voided samples from mares.

Delays in examination, especially at room temperature, usually cause artifactual degeneration in cells and allow bacterial proliferation. Usually, however, specific cell types can be identified. Samples should be collected fresh so far as is possible and should be collected into a sterile container. The sample should be stored in a refrigerator at 4°C until analysis can be performed. Urinary infection is usually indicated by high numbers of neutrophil leukocytes in urine but this does not indicate specifically if the origin is renal, ureteral or the bladder. It can be difficult to differentiate contaminant (incidental) bacteria from pathogens in samples that have been stored for more than 12 h even if they have been refrigerated. Where cytology only is required, a drop or two of 10% formalin solution can be added to the urine to maintain cell structure. This, however, will clearly completely negate any attempt at culture.

Erythrocytes and ghost cells will be seen in cases of hematuria (q.v.) even if a degree of hemolysis has occurred in the urinary tract or after collection of the sample. Grossly abnormal cells, including neoplastic and extensive sheets of transitional or cuboidal epithelial cells, indicate severe abnormality.


Gamma glutamyltransferase (GGT) is found in the liver, pancreas and luminal brush border of the proximal tubular cells. This enzyme is not excreted by glomerular filtration, so when it is detected in urine it is strongly indicative of tubular damage. Because it appears before azotemia develops, it is a sensitive indicator of early (acute) renal tubular disease such as acute tubular necrosis (q.v.).

Urinary GGT concentrations are conventionally expressed as a ratio to urinary creatinine concentrations to compensate for variations in urine flow rate at the time of sampling:


Horses with renal compromise have values >25 but urinary GGT values fall once the acute insult has ceased, despite persistent tubular dysfunction. The value of this assay in progressive or chronic renal failure is therefore doubtful.


In health the glomerular filtration rate (GFR) remains remarkably constant due to the intrarenal regulatory mechanisms; the net urinary excretion of an electrolyte is governed by GFR and the efficiency of tubular resorption. GFR can be measured by several methods including clearances of endogenous creatinine or exogenous inulin, or radionuclide (99 mTc-DTPA) or plasma disappearance of sodium sulfanilate, phenolsulfonphthalein or radiolabeled compounds. Certain drugs such as the potentiated sulfonamides reduce tubular secretion of creatinine and so may induce a rise in serum creatinine and a fall in measured clearance.

Creatinine is excreted by filtration alone and its rate of excretion therefore provides a good indicator of the GFR, even during renal dysfunction. The only practical method of measuring (estimating) the GFR in horses with normal or near normal renal function is through measurement of the creatinine clearance. Urea is not a useful parameter to use to calculate GFR.

The normal GFR of horses is between 1.6 and 2.0 mL/min/kg and this must be reduced by 60–75% to result in a detectable increase in serum urea and creatinine concentrations. Measurement of the circulating concentrations of creatine and urea are relatively insensitive indicators of renal function because they change relatively slowly with time.

A pathologic reduction in intrarenal blood flow, glomerular damage or loss, or obstruction to the free flow of ultrafiltrate along the renal tubular system causes the GFR to fall, and with it the ability of the kidney to eliminate waste material and to regulate the volume and composition of body fluid will decline. This is manifest as a rise in blood urea and creatinine concentrations and a reduction in the measured GFR.

There is no convenient method of collecting total urine voided by ambulatory foals or mares, but urine output can be collected in male horses by placing a urine collection device around the abdomen. When monitoring urine output in critically ill foals and mares is desired, it can be accomplished by use of an indwelling Foley catheter and urine collection bag (closed system). The risk of ascending infection can be reduced by placing a one-way valve (such as the cut off finger of a surgical glove) over the end of the catheter to prevent aspiration of air and bacteria.


Creatinine clearance is a useful standard against which the clearance of an electrolyte may be compared in health or disease. The fractional excretion (FE) of an electrolyte is defined as the per cent ratio of its clearance to the clearance of endogenous creatinine. In normal homeostatic balance, FE values vary with dietary and water intake variations, but usually fall within a definable range. With a loss of tubular resorption the excretion of an electrolyte is often increased and its FE rises above the normal range. The FE is derived as follows:


divided by


which can be simplified to:


The FE of an electrolyte is therefore calculated from urinary and plasma concentrations of the electrolyte and creatinine. The FE ranges for healthy horses are shown in Table 12.3.

In general terms, a persistent increase in the FE of one or more electrolytes (frequently sodium and phosphorus) is suggestive of tubular dysfunction but there are a number of caveats to the interpretation of results of FE calculations:



Special considerations of renal function in the foal

The fetal urinary tract is immature and has limited control of fluid and electrolyte balance and removal of nitrogenous waste products; the fetus relies heavily (but not exclusively) on the placenta.

Normal colt foals will void a normal stream of urine within 4 h of birth while the first urination of filly foals is often delayed up to 6 h. This has implications for the detection of patency of the urinary tract (q.v.). Mature renal function is not achieved for several weeks after birth. Foals often have a transient proteinuria for the first 2–3 days as a result of filtration of small molecular weight proteins absorbed with colostral protein. The high dietary fluid intake results in acidic urine of low specific gravity (1.001–1.004), low osmolarity and high volume (148 mL/kg/day, i.e. up to 6–7L/day). A few epithelial cells and calcium oxalate crystals may be present in normal foal urine. However, the presence of erythrocytes, leukocytes, casts, hemoglobin or myoglobin in foal urine is always abnormal.

Serum creatinine elevations in neonatal foals

In the first 1–3 days, creatinine concentrations are often in the range 141–194μmol/L. This gradually falls to 88–106μmol/L over the first 2–3 wk as renal function matures. The likely cause is an inability of creatinine to equilibrate across placental membranes. A mildly elevated creatinine concentration in an otherwise healthy foal (that has urinated normally) is therefore probably of little concern. However, if the concentration does not decline over 3–4 days or remains >200μmol/L on day 3, then peritoneal or retroperitoneal accumulation of urine, renal hypoplasia or other causes of renal failure should be considered (q.v.).

Unlike creatinine, blood urea concentrations in foals are typically low (<5μmol/L) after day 2 and remain low for the first several months of life. This finding can be attributed to the anabolic state of the growing foal.

The trend in creatinine and urea concentrations in azotemic foals should be closely monitored; a continued increase would suggest renal dysfunction and demands additional evaluation.


Congenital defects in the foal are rare apart from patent urachus (q.v.) and failure of the normal fusion of the urinary bladder (q.v.). Reported defects include renal agenesis, polycystic kidneys, renal glomerular hypoplasia and ectopic ureters (q.v.). Various dysplastic conditions (where the renal structure has a chaotic or disorganized nature) also occur.

The age of onset of relevant clinical signs is dependent on the degree of renal pathology and the extent of loss of function. In some cases the conditions are fully compatible with life and are only detected incidentally at post mortem examination at a later age; in others clinical signs are delayed until 6–18 mo although some evidence can usually be found before that.

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Jul 8, 2016 | Posted by in EQUINE MEDICINE | Comments Off on The urinary system
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