Bryan M. Waldridge
Polyuria and Polydipsia
Polyuria and polydipsia (PU/PD), defined by inappropriately high urine production and water intake, respectively, are common presenting complaints in equine medicine. Generally, history, physical examination, and routine clinicopathologic tests such as complete blood count, serum chemistry, and urinalysis will readily rule out many of the differential diagnoses discussed in this chapter (Box 103-1). Assessment of renal function is an important first step in the diagnostic workup of horses with PU/PD and allows the clinician to better formulate a differential diagnosis list and pursue other necessary diagnostic procedures.
Differential Diagnoses
Psychogenic Water Drinking
Psychogenic water drinking is the most common cause of PU/PD in horses. Horses that are kept in stalls most of the day and meal fed, with limited access to pasture and hay, are most likely to develop psychogenic water drinking and PU/PD. Psychogenic water drinking can be considered a stable vice because it develops in horses that are largely stall-confined and do not have constant access to forage. Boredom leads the horse to continuously drink water and subsequently urinate. Horses with psychogenic water drinking are able to produce concentrated urine if water intake is restricted. Treatment of psychogenic water drinking involves providing activities to relieve boredom and restore a more normal equine lifestyle, such as turning the horse out as much as possible, feeding small and frequent concentrate meals rather than only two meals per day, and providing forage at all times when the horse is stalled.
Iatrogenic (Drug or Fluid Therapy-Induced) Polyuria
Intravenous or orogastric fluid therapy delivered at greater than maintenance rates will increase urine production if urinary tract function is normal. Corticosteroids decrease secretion of antidiuretic hormone (ADH) and increase output of dilute urine. α2-Agonist sedatives decrease secretion of both ADH and insulin. Hyperglycemia from α2-agonist–induced hypoinsulinemia may persist for up to 150 minutes after administration, although glycosuria is uncommon and is not likely to induce osmotic diuresis.
Endocrine Disease
Pituitary Pars Intermedia Dysfunction and Equine Metabolic Syndrome
Horses with pituitary pars intermedia dysfunction (PPID) or equine metabolic syndrome (EMS) have PU/PD because of hypercortisolemia and hyperglycemia that may exceed renal threshold. Cortisol inhibits ADH, resulting in increased output of dilute urine. Most horses with PPID or EMS are not sufficiently hyperglycemic to exceed renal threshold. Horses with PPID are generally older, but PPID has been diagnosed in horses as young as 7 years. Many horses with PPID have few clinical signs other than hypertrichosis and PU/PD. Equine metabolic syndrome develops in younger (generally 5 to 15 years old) obese horses with abnormal fat deposits. Affected horses tend to have recurrent laminitis.
Specific endocrine testing such as the dexamethasone suppression test, combined dexamethasone suppression and thyrotropin-releasing hormone response test, and measurement of blood glucose, insulin, cortisol, and adrenocorticotrophic hormone concentrations aid in the diagnosis and differentiation of PPID and EMS. Equine metabolic syndrome and PPID are discussed in detail in Chapters 135 and 136, respectively.
Diabetes Insipidus
Antidiuretic hormone (arginine vasopressin) acts on the distal renal tubules and collecting ducts to increase permeability to water, which causes water to reenter the circulation. This effect concentrates urine and conserves body water. Central or neurogenic diabetes insipidus is caused by hypothalamic or pituitary dysfunction and decreased ADH production or release. Nephrogenic diabetes insipidus occurs when the medullary collecting ducts cannot conserve water in response to ADH. Both nephrogenic and central diabetes insipidus are uncommon in horses. Nephrogenic diabetes insipidus has been reported in colts, two of which were full siblings. This suggests that in some instances nephrogenic diabetes insipidus may be inherited as a sex-linked trait, as has been reported in other species. Some colts with nephrogenic diabetes insipidus have been described as small in size and thin, compared with others. Acquired diabetes insipidus can be idiopathic or the result of trauma, vascular abnormalities, encephalitis, or neoplasia. In one case, urinary overflow incontinence was confirmed to be caused by acquired nephrogenic diabetes insipidus. Some authors associate diabetes insipidus and PPID with hypertrophy of the pars intermedia, pressure on the posterior pituitary gland, and decreased ADH release.
One colt with nephrogenic diabetes insipidus was successfully treated with dietary salt restriction; salt was limited to that which was contained in the feed and forage. Water intake was also restricted by offering water five to six times per day. The colt gained weight and maintained normal clinicopathologic values but continued to produce dilute urine.
In another case report, congenital central diabetes insipidus was suspected in a 10-day-old colt examined for polyuria and tachypnea. However, the foal had plasma vasopressin concentrations that were very similar to those in age-matched controls. The colt was treated with desmopressin acetate hydrate ophthalmic drops, and urine specific gravity increased from 1.012 to 1.019. The foal’s plasma vasopressin concentrations increased after ocular administration, which indicates that ophthalmic desmopressin products are absorbed and could potentially be efficacious to treat central diabetes insipidus. Twenty-four months later, the colt had grown normally but still could not produce concentrated urine.
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