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: Central diabetes insipidus (DI) was diagnosed in a 20-year-old American Quarter Horse gelding that was concomitantly affected with pituitary pars intermedia dysfunction (PPID). The diagnosis of DI was supported by a positive response to administered desmopressin acetate. Diagnosis of PPID was supported by physical appearance and elevated plasma adrenocorticotropic hormone concentration following domperidone administration. The horse's physical condition improved following treatment with pergolide but long-term treatment with desmopressin was not undertaken and severe polyuria and polydipsia persisted. Desmopressin acetate appears to be useful for the diagnosis of DI in mature horses concomitantly affected with PPID.Equine Veterinary Education. 03/2013; 25(3).
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ABSTRACT: Aquaporin-2 (AQP2), the vasopressin-regulated water channel of the renal collecting duct, is dysregulated in numerous disorders of water balance in people and animals, including those associated with polyuria (urinary tract obstruction, hypokalemia, inflammation, and lithium toxicity) and with dilutional hyponatremia (syndrome of inappropriate antidiuresis, congestive heart failure, cirrhosis). Normal regulation of AQP2 by vasopressin involves 2 independent regulatory mechanisms: (1) short-term regulation of AQP2 trafficking to and from the apical plasma membrane, and (2) long-term regulation of the total abundance of the AQP2 protein in the cells. Most disorders of water balance are the result of dysregulation of processes that regulate the total abundance of AQP2 in collecting duct cells. In general, the level of AQP2 in a collecting duct cell is determined by a balance between production via translation of AQP2 mRNA and removal via degradation or secretion into the urine in exosomes. AQP2 abundance increases in response to vasopressin chiefly due to increased translation subsequent to increases in AQP2 mRNA. Vasopressin-mediated regulation of AQP2 gene transcription is poorly understood, although several transcription factor-binding elements in the 5' flanking region of the AQP2 gene have been identified, and candidate transcription factors corresponding to these elements have been discovered in proteomics studies. Here, we review progress in this area and discuss elements of vasopressin signaling in the collecting duct that may impinge on regulation of AQP2 in health and in the context of examples of polyuric diseases.Veterinary Clinical Pathology 11/2012; · 1.29 Impact Factor
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ABSTRACT: A 14-year-old Cleveland Bay cross gelding was presented with severe urinary incontinence that had been present for 1 year, and chronic polydipsia and polyuria over 4 years. Water intake had been recorded as 240 L over a 24-hour period. The horse had marked urinary incontinence and polyuria and polydipsia. The urine was markedly hyposthenuric, but no abnormalities on urinalysis were detected. There were no other abnormal clinical or neurological signs. Haematological and serum biochemical examinations showed no abnormalities and ultrasonographic and endoscopic examination of the urinary tract did not reveal any abnormalities. The horse underwent a modified water deprivation test and failed to concentrate its urine after 5 days. 1-desamino-8-d-arginine vasopressin (DDAVP) was administered I/V but the urine remained isosthenuric with a specific gravity of 1.010. Nephrogenic diabetes insipidus. A definitive cause of the urinary incontinence was not found but overflow incontinence was considered a possibility. Despite being a rare condition in the horse diabetes insipidus should be considered in cases of severe polydipsia and polyuria in mature horses.New Zealand veterinary journal 07/2012; 60(4):254-7. · 1.06 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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