Polyuria and polydipsia in horses.
ABSTRACT Polyuria and polydipsia provide a diagnostic challenge for the equine clinician. This article describes the various known causes of polyuria and polydipsia in horses and provides a description of a systematic diagnostic approach for assessing horses with polyuria and polydipsia to delineate the underlying cause. Treatment and management strategies for addressing polyuria and polydipsia in horses are also described.
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ABSTRACT: The components of the daily external water and electrolyte balances of five normal Standardbred geldings with a mean body weight of 427 kg, were determined over 14 day periods. The mean value of daily total water intake (a summation of free, combined and metabolic water intake) for the group was 27.6 litres, that is, 64.4 ml/kg body weight, while mean values for ambient temperature and humidity ranged from 16 to 25°c and 55.4 to 75.5 per cent, respectively. the mean daily urine volume of 9.9 litres (23.2 ml/kg) for the group, was found to exceed the mean faecal water output of 7.2 litres (16.9 ml/kg). the mean output of sodium for the five animals, in urine and faeces, was 780 mmol or 79 per cent of the intake. the mean output of potassium, chloride, calcium and magnesium were 3163, 2521, 1824 and 1448 mmol or 95, 84, 74 and 75 per cent, respectively of intake. the sodium and potassium not accounted for in urine and faeces may well have been lost in sweat. results are discussed and compared with those of a previous external balance study in the horse.Equine Veterinary Journal 04/1988; 20(3):189 - 193. · 2.29 Impact Factor
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ABSTRACT: The objectives of this study were to: 1) determine incremental and total sweat fluid and ion losses during and following (a) exercise training and (b) a treadmill Speed and Endurance exercise test (SEET) which simulated running speeds and distances required for each phase of an Olympic level (CCI****) 3-day-event in cool and hot ambient conditions and 2) determine the requirement for ion supplementation based on the calculated ion losses associated with these activities. Six exercise-trained Thoroughbred horses completed 2 weeks of exercise training in each of 2 ambient conditions: cool, dry (CD, room temperature [T] = 20-22 degrees C, relative humidity [RH] = 45-55%), or hot and humid (HH, T = 33-35 degrees C, RH = 80-85%). Following the 2 week period of training in either CD or HH conditions, horses completed a SEET under similar conditions (either CD, or hot and dry (HD, T = 33-35 degrees C, RH = 45-55%). Sweating rate and sweat ion composition for each 5 min interval was determined from sweat samples collected from a sealed pouch attached to the lateral thorax. Total sweat fluid losses during training in the heat were 2- or 3-fold greater when compared to CD. Similarly, sweat fluid losses associated with the SEET in HD were almost double (19.2 litres) the losses in CD (11.7 litres). Total calculated ion losses associated with 2 h of training in HH (3724 mmol; 115.2 g) were significantly greater when compared to CD (1413 mmol; 43.5 g). Following the SEET and a 30 min recovery period, total ion losses in CD were 3636 mmol (112.2 g) compared with 6519 mmol (200.6 g) in HD. The differences in ion losses represent the increased sweating rates stimulated by higher core temperatures during moderate to high intensity exercise in warmer ambient conditions and increases in sweat ion concentrations associated with higher sweating rates. Extracellular fluid (ECF) ion losses during daily exercise training and the SEET were also calculated from changes in plasma ion concentrations and ECF volume. Calculated ECF ion losses were significantly higher in hot ambient conditions but were approximately 50% less than calculated sweat ion losses. The calculated sweat ion losses incurred during daily exercise training in hot and humid ambient conditions are > 3-fold higher than losses measured following exercise training in cooler conditions. Whereas fluid regulating hormones may have reduced urinary and faecal losses of ions during 2 weeks of training in HH, the quantity of sodium, potassium and chloride calculated to have been lost in sweat during the SEET in HD exceeded the daily dietary intake of these ions and suggests the need for appropriate ion supplementation during training and competition in hot ambient conditions.Equine veterinary journal. Supplement. 08/1996;
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ABSTRACT: The stimuli that elicit thirst were studied in four ponies. Nineteen hours of water deprivation produced an increase in plasma protein from 67 +/- 0.1 g/litre to 72 +/- 2 g/litre, a mean (+/- se) increase in plasma sodium from 139 +/- 3 to 145 +/- 2 mmol/litre and an increase in plasma osmolality from 297 +/- 1 to 306 +/- 2 mosmol/litre. Undeprived ponies drank 1.5 +/- 0.9 kg/30 mins; 19 h deprived ponies drank 10.2 +/- 2.5 kg/30 mins and corrected the deficits in plasma protein, plasma sodium and plasma osmolality as well as compensating for the water they would have drunk during the deprivation period. In order to determine if an increase in plasma osmolality would stimulate thirst, 250 ml of 15 per cent sodium chloride was infused intravenously. The ponies drank when osmolality increased 3 per cent and when plasma sodium rose from 136 +/- 3 mmol/litre to 143 +/- 3 mmol/litre. Ponies infused with 15 per cent sodium chloride drank 2.9 +/- 0.7 kg; those infused with 0.9 per cent sodium chloride drank 0.7 +/- 0.5 kg. In order to determine if a decrease in plasma volume would stimulate thirst, ponies were injected with 1 or 2 mg/kg bodyweight (bwt) frusemide. Plasma protein rose from 68 +/- 2 g/litre pre-injection to 75 +/- 2 g/litre 1 h after 1 mg/kg bwt frusemide and to 81 +/- 1 g/litre 1 h after 2 mg/kg bwt frusemide.(ABSTRACT TRUNCATED AT 250 WORDS)Equine Veterinary Journal 02/1985; 17(1):12-6. · 2.29 Impact Factor
Polyuria/Polydipsia in Horses
Oregon State University, Corvallis, OR, USA
OBJECTIVES OF THE PRESENTATION
To review the various causes of polyuria/polydipsia in the horse, to construct a systematic diagnostic
approach to the problem, and to review management and treatment options.
KEY ETIOLOGIC AND PATHOPHYSIOLOGIC POINTS
Psychogenic polydipsia (excessive voluntary intake of water) is a common cause of polyuria in the horse.
However, the clinician should only make this diagnosis after ruling out more serious causes of increased
Normal horses consume 25 to 70 ml/kg of bodyweight in water each day, much of which is
consumed in food, and the remainder derived from metabolic processes and water consumption.1 The
amount of water consumed by an individual horse may vary dramatically and will be influenced by
factors including diet composition, environmental conditions and physiologic demands such as exercise
The majority of water consumption in non-pasture kept horses occurs within 30 minutes after
eating, with approximately 3 to 4 liters of water consumed per kilogram of hay. Water requirements are
higher for horses consuming hay versus concentrate-based rations because the lower digestibility of hay
increases fecal mass and moisture content.2 Horses consuming grass may not require additional water,
although they will likely drink it if it is made available to them. Inadequate water consumption can
detrimentally effect performance and feed intake.2 Conservation of water within the body is largely
dependant on the actions of antidiuretic hormone (ADH) which promotes absorption of water in the
distal renal tubule and collecting ducts of the kidney.4,5 Failure to produce or release ADH, or failure of
the renal tubules to appropriately respond to ADH for a variety of reasons may result in excessive water
loss and compensatory polydipsia.
Normal horses produce 15–30 ml/kg of bodyweight in urine per day (approximately 5 to 15 L per
day.1,6 Foals produce relatively greater urine volumes (148 ml/kg of bodyweight per day) as a result of
physiologic hyposthenuria for the first 6–8 weeks of life.7
Polydipsia is classified as consumption of more water than 100 ml/kg of bodyweight per day (50L
for an average size 500 kg adult horse) and polyuria as production of more than 50 mL/kg of bodyweight
in urine per day (25 L for an average horse).8 However, factors that influence water intake must be
considered, including colonic disease or exercise in hot weather which may result in water consumption
approaching 100 L per day or more. However, physiologic polydipsia should not result in polyuria, since
the water consumed should be directed towards the initiating requirements. Therefore when
investigating polyuria/polydipsia, it is critical to combine objective measurements of water consumption
and/or urine production with thorough assessment of all factors that may influence water requirement.
Causes of Polydipsia and Polyuria in Horses
Primary polydipsia: A behavioral tendency to consume excessive amounts of water (psychogenic
polydipsia) is one of the most common causes of excessive water consumption in horses and usually
results in secondary polyuria.9 This condition is most frequent in mature stabled horses, and is often
severe.10 Usually no other abnormalities can be identified aside from polyuria/polydipsia, and urine will
be hyposthenuric (specific gravity < 1.005).8,11Chronic psychogenic polydipsia can lead to loss of
electrolytes from the interstitium of the kidney, which can ultimately impair renal concentrating ability
and may interfere with diagnostic testing, particularly assessment of responses to water deprivation.
Although excessive salt consumption has been blamed for polydipsia in some horses, a very large
amount of salt needs to be consumed to promote polydipsia (minimum of 5% of dry matter intake) which
few horses are likely achieve.8
81st Western Veterinary Conference
Pathologic polyuria: In horses without primary polydipsia, excessive water consumption is likely to
reflect compensation for pathologic polyuria. Pathologic polyuria may result from primary renal
dysfunction such as renal failure and nephrogenic diabetes insipidus in which the renal tubules do not
respond to antidiuretic hormone.12,13 Systemic causes of polyuria include Pituitary Pars Intermedia
Dysfunction (PPID; Equine Cushing’s), neurogenic (central) diabetes insipidus, diabetes mellitus and
endotoxemia.8,10 Iatrogenic causes include administration of intravenous fluids, corticosteroids, diuretics
and alpha 2 agonist drugs.8,10
Chronic renal failure: This is not an uncommon cause of polyuria in horses. A decline in the number
of functional nephrons overwhelms the absorptive capacity of remaining nephrons, subsequently
resulting in solute and water loss.11Causes of chronic renal failure in horses include congenital
abnormalities (renal dysplasia, polycystic kidney disease), pyelonephritis, glomerulonephritis,
amyloidosis, urinary obstruction and neoplasia. Chronic renal failure may also represent
progression of acute renal failure initiated by shock, toxins, pigmenturia, severe endotoxemia, and
Nephrogenic diabetes insipidus occurs when renal tubules cannot respond to ADH. Affected
animals do not concentrate their urine in response to water deprivation or the administration of an
exogenous source of ADH.14 Although rare in horses, primary nephrogenic diabetes insipidus has
been described in two related Thoroughbreds with profound polydipsia.13 These horses developed
dehydration during water restriction and their urine specific gravity did not increase after they
were given exogenous ADH. However, one horse displayed an increase in endogenous plasma
ADH concentration during water restriction, indicating a renal rather than central problem. It
should be recognized that it horses commonly display decreased renal responsiveness to ADH as a
secondary event associated with underlying renal failure or endocrine and metabolic disorders.14,15
Central diabetes insipidus results from failure of production or release of ADH. Affected horses are
likely to display profound polydipsia and polyuria with hyposthenuric urine.4,16 In other species,
central DI may be congenital, idiopathic, or associated with trauma, intracranial neoplasia and
inflammatory diseases.14 Central DI very rarely occurs in horses, but has been described with
encephalitis and as an idiopathic occurrence.17,18 Affected horses cannot increase plasma ADH
concentrations or increase urine SG when deprived of water, but they can concentrate their urine if
an exogenous source of ADH is given.
Pituitary Pars Intermedia Dysfunction commonly causes polyuria and polydipsia in affected horses.
It is possible these signs reflect a form of central DI due to impingement of the abnormal pars
intermedia tissue on the hypothalamus and pituitary interfering with ADH production and/or
release.19 Additional contributing factors could include glucosuria creating osmotic diuresis, and
decreased renal sensitivity to ADH as a consequence of elevated plasma cortisol concentrations.8,10
Although glucosuria, hyperglycemia and polydipsia/polyuria should be considered strongly
suggestive of PPID, diabetes mellitus has also been reported to create similar clinical signs in
Miscellaneous disorders that may be associated with PD/PU in horses include septic conditions
such as peritonitis and liver disease.
Diagnostic assessment of polydipsia/polyuria: It is critical that diagnostic testing occur in a systematic
and careful manner to avoid inappropriate water deprivation testing which may exacerbate underlying
Collect a detailed history: Include duration of the problem, recent management changes, medication
history, appetite and ration composition including supplements.
Physical examination should include assessment of hydration status and per rectum examination of
the urinary tract. Horses with psychogenic polydipsia should appear healthy. Poor body condition,
lethargy and a poor hair coat are suggestive of chronic renal failure. Horses with PPID commonly
have an abnormal hair coat and may have a history of chronic infections and laminitis.10,21
Objective measurement of water consumption should be performed to confirm that PD truly exists.
Horses should be stall confined and their consumption of water from a single non-automated water
source measured periodically throughout a 24 hour period. Estimates of water loss through spilling
and splashing may be required. Horses with psychogenic polydipsia or diabetes insipidus often
consume large quantities of water and produce large amounts of dilute urine.9,13 Renal failure and
PPID usually have less profound effects on water consumption and urine production.
Measurement of urine volume is more complicated but should be undertaken if possible. All
methods of urine quantification require stall confinement, cross tying where appropriate, and close
observation. Indwelling Foley catheters can be used to collect urine into a bag in mares. Urine
collection harnesses can be used on both genders.
A CBC and serum biochemistry panel (including BUN, creatinine and glucose) should be
performed with concurrent analysis of a urine sample including measurement of SG, dipstick
analysis for glucose, protein and pigment content, and microscopic examination of urine sediment.
A urine sample can be readily obtained from the mare by passing a uterine pipette a few
centimeters into the urethra with sterile technique, then aspirating with a syringe. Free catch
samples are ideal in geldings and stallions since the administration of most sedative agents will
alter urine characteristics.
Hyposthenuria (SG < 1.007) indicates that renal failure and complete medullary washout
are unlikely since renal diluting capability is intact.4,10 However, since horses can display
hyposthenuria rather than isosthenuria during recovery from acute renal failure, renal
failure should only be discounted after appropriate diagnostics.8
Horses with psychogenic PD have hyposthenuria and no other laboratory abnormalities.
Horses with PPID may display hyperglycemia, mild neutrophilia and lymphopenia.
Glucosuria may also occur, but can also occur with non-PPID associated diabetes
mellitus and possibly renal tubular dysfunction. PPID should be confirmed via a
dexamethasone suppression test.22
Azotemia in conjunction with isosthenuria (urine SG 1.008–1.014) indicates the loss of
approximately 75% of functional nephrons.19 Hypercalcemia and hypophosphatemia are
frequent signs of renal disease in horses.
Suspected renal disease should be further assessed via transrectal ultrasound of the left kidney and
urinary tract, and transabdominal ultrasound of both kidneys. Ultrasound-guided renal biopsy
should be performed if renal disease is suspected.
Water Deprivation Testing: This diagnostic is reserved for differentiating nephrogenic and central
diabetes insipidus from psychogenic polydipsia. Therefore it should be applied only after renal
disease has been ruled out, and is usually indicated when hyposthenuria is present.4,14 Water
deprivation testing should not be performed in horses with azotemia or dehydration.
In healthy horses, water deprivation will increase plasma osmolality causing ADH
release and a corresponding increase in urine SG and osmolality. After 48 hours of water
deprivation, urine SG values should exceed 1.040 in a healthy horse.24,25
After obtaining preliminary urine and blood samples, the bladder should be emptied and
a baseline bodyweight obtained. The horse is confined without water, and bodyweight,
urine SG and potentially plasma BUN and creatinine are measured every 2–4 hours.26
Normal horses will increase urine SG to >1.025 after 24 hours, or once 5% of bodyweight
has been lost.11 The test should be terminated once an appropriate urine SG is reached, if
the horse’s bodyweight decreases by 5%, or if dehydration or azotemia occur.
Horses with psychogenic PD will increase urine SG when deprived of water if they do
not have medullary washout. Horses with chronic psychogenic polydipsia may not be
able to increase urine SG above 1.020 with abrupt water deprivation. In such cases water
intake can be restricted to 40 ml/kg/bodyweight per day for 3–4 days with frequent
assessment of hydration status and urine SG. This approach should result in a urine SG
>1.025 by the end of the testing period.10,11
Horses that produce a urine SG between 1.008 and 1.020 with abrupt or modified water
deprivation may have partial central DI or renal insufficiency and require further
evaluation for these conditions.4,27 Horses with complete central or nephrogenic DI will
continue to pass urine with a low SG (< 1.008) and will display a progressive loss of
bodyweight. Distinguishing between central and nephrogenic DI can be accomplished by
administering synthetic ADH or ADH analogues such as desmopressin acetate (DDAVP)
and monitoring subsequent changes in urine SG. 27 DDAVP can be administered by
diluting the nasal spray formulation (0.1 mg/ml) in sterile water and administering 0.05
ug/kg IV. Urine SG should be measured every 2 hours, and an increase in SG to 1.025 or
greater within 2 to 7 hours is consistent with central DI. No change in urine SG is
consistent with nephrogenic DI if medullary washout has been accounted for.26
Management of Polydipsia/Polyuria
Affected horses can be difficult to care for in a stabled environment. Psychogenic polydipsia usually
reflects boredom and therefore environmental enrichment techniques such as the provision of toys,
providing a constant forage supply, or pasture turnout are often helpful. Horses with psychogenic
polydipsia should be provided daily with the volume of drinking water considered appropriate to meet
their estimated requirements, only after pathologic causes of polydipsia/polyuria have been excluded.28
Horses with a tendency for excessive salt consumption should not be allowed access to free-choice
mineral sources, and their feed can be top-dressed with an appropriate mineral supplement to meet their
estimated mineral requirements.
Horse with renal dysfunction or nephrogenic or central DI should be given completely unrestricted
access to an unlimited fresh water supply to avoid dehydration or exacerbation of renal dysfunction.
Automated water sources might be better avoided in case of catastrophic malfunction. Electrolyte and
mineral supplementation (particularly with sodium and chloride) may be required to compensate for
urinary losses of these electrolytes, although calcium intake should be restricted in horses in renal failure
to avoid exacerbating hypercalcemia. Therefore feed stuffs such as alfalfa hay should be avoided, and
commercial mineral supplements carefully selected. Periodic monitoring of plasma electrolyte and
mineral concentrations, BUN and creatinine should be performed and a palatable high energy diet
Specific treatment of central diabetes insipidus using exogenous vasopressin or desmopressin is
performed successfully in small animals but has not been described in the horse. Treatment of horses
would likely be cost prohibitive and the efficacy of such treatment is currently unknown.
Polyuria in horses with PPID may respond to treatment with dopamine agonists including
bromocriptine or pergolide.10 Trilostane, a competitive inhibitor of 3-beta hydroxysteroid dehydrogenase
used to treat canine pituitary dependant hyperadrenocorticism has been reported to improve polyuria
and polydipsia and other clinical signs of PPID in affected horses.29
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