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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • PU—urine output >50 mL/kg/day
  • PD—fluid intake >100 mL/kg/day

Pathophysiology!!navigator!!

  • Production of concentrated or dilute urine requires generation of the interstitial concentration gradient from the renal cortex to the inner medulla, dilution of tubular fluid in the thick ascending limb of the loop of Henle and distal tubule (diluting segment of the nephron that has low water permeability), and presence or absence of water channels in the collecting ducts (controlled by ADH activity)
  • Modest increases in plasma tonicity (≅3 mOsm/kg) stimulate production and release of ADH by the posterior pituitary gland and insertion of aquaporins (water channels) in the luminal membrane of collecting duct epithelial cells, leading to increased water permeability and reabsorption
  • Decreases in plasma tonicity inhibit ADH release and insertion of aquaporins. As a result, collecting ducts become less permeable to water, and dilute urine is produced
  • Transient PU may be an effect of fluid or drug administration (e.g. furosemide and other diuretic agents) or a consequence of loss of the medullary concentration gradient—medullary washout
  • Persistent PU is generally associated with a number of disease processes—CKD, PPID, DI, DM, and endotoxemia
  • There are 2 important stimuli for thirst—an increase in plasma tonicity and hypovolemia
  • PD may be a physiologic response to PU (to prevent dehydration), a consequence of drug administration (e.g. corticosteroids), or a primary problem of excessive water intake
  • Urine production and water consumption vary with age, diet, workload, environmental temperature, and gastrointestinal water absorption

Systems Affected!!navigator!!

  • Renal/urologic—excessive urine production
  • Endocrine/metabolic—PPID; DM
  • Nervous—central DI
  • Behavioral—excessive water intake, excessive salt consumption

Genetics!!navigator!!

Unknown—familial nephrogenic DI in Thoroughbred colts.

Incidence/Prevalence!!navigator!!

PPID may affect up to 15% of horses >20 years of age.

Signalment!!navigator!!

Breed Predilections

PPID appears to be more common in Morgan horses and ponies.

Mean Age and Range

PPID occurs in older horses and ponies.

Predominant Sex

Familial nephrogenic DI in Thoroughbred colts.

Signs!!navigator!!

Historical Findings

  • Horses with mild to moderate PU/PD often go undetected by owners, or the horse may stop to urinate while being ridden or have excessive thirst after exercise
  • With more substantial PU/PD (e.g. with primary PD), the magnitude of PU typically is dramatic, with owners reporting that horses drink 2–3-fold more water and that stalls can be flooded with urine
  • Horses with acquired DI may have a recent history of medical problems or treatment with a potentially nephrotoxic medication

Physical Examination Findings

Consistent with the underlying disease processes (e.g. CKD, PPID) or normal (e.g. primary PD, excessive salt ingestion).

Causes!!navigator!!

Primary PD

  • Primary or “psychogenic” PD probably is the most common cause of PU/PD in adults
  • The cause is unknown; however, in some horses it appears to be a stable vice, while in others it may develop after a change in management (e.g. stabling, diet, interaction with other horses, or medication administration)

Excessive Salt Consumption

“Psychogenic salt eaters” appear to be less common than those with primary PD; salt intake may have to exceed 5–10% of dry matter intake before PU/PD becomes apparent.

Drug Administration

Administration of enteral or IV fluids, diuretics, α2-agonists, and corticosteroids.

CKD

  • These horses cannot concentrate urine beyond the isosthenuric range (specific gravity 1.008–1.014)
  • The degree of PU is modest compared with primary PD or DI, so it is a client complaint only in ≅50% of affected horses

PPID

  • An osmotic diuresis when plasma glucose concentration exceeds the renal threshold, leading to glucosuria
  • Antagonism of the action of ADH on collecting ducts by cortisol
  • A primary dipsogenic effect of excessive cortisol
  • Compression of the posterior pituitary by growth of an adenoma leading to central DI

DI

  • May occur because of inadequate secretion of ADH (neurogenic or central DI) or decreased sensitivity of the epithelial cells of the collecting ducts to circulating ADH (nephrogenic DI)
  • An acquired form of central DI has been described in horses and is idiopathic or secondary to encephalitis or other diseases accompanied by dehydration, endotoxemia, or administration of potentially nephrotoxic medications

DM

A state of chronic hyperglycemia accompanied by glucosuria resulting in an osmotic diuresis.

Sepsis/Endotoxemia

PU/PD occasionally is observed in horses with sepsis or endotoxemia. The mechanism is unclear but may result from endotoxin-induced prostaglandin production. Prostaglandin E2 is a potent renal vasodilating agent that also can antagonize the effects of ADH.

Risk Factors!!navigator!!

See chapters listed in See Also.

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

CBC/Biochemistry/Urinalysis!!navigator!!

  • CKD, PPID, sepsis/endotoxemia—see chapters listed in See Also
  • Primary PD and DI—CBC and serum chemistry results are normal, but USG typically is <1.005
  • DM—hyperglycemia and glucosuria are present

Other Laboratory Tests!!navigator!!

  • Measurement of fractional sodium clearance in horses with primary PD. It is increased (>1%) when excessive salt intake is the cause
  • Measurement of plasma ADH concentration would be useful in cases of DI to differentiate neurogenic (low ADH) from nephrogenic (high ADH when dehydrated) forms, but this assay is not commercially available

Imaging!!navigator!!

Transabdominal/transrectal ultrasonography—to assess kidney size and echogenicity (should be normal, except with CKD).

Other Diagnostic Procedures!!navigator!!

  • Overnight water deprivation is the most useful test to determine ability to concentrate urine. Horses with primary PD should concentrate urine to a specific gravity of 1.020–1.025; horses with CKD and DI fail to concentrate urine
  • Approach water deprivation cautiously in horses with suspected DI, and do not perform when azotemia is detected (CKD). Measure body weight before water deprivation; do not extend the test beyond the time needed to lose 5% of body weight (may be <12 h in horses with DI)
  • Horses are suspected to have DI when they fail to concentrate urine during water deprivation. Administration of desmopressin acetate (DDAVP; 0.1 mg/mL solution diluted in sterile water and 0.05 mg/kg, can be administered IV for this purpose) can be used to differentiate neurogenic DI (will concentrate urine to >1.020) from nephrogenic DI (will not concentrate urine)

Treatment ⬆ ⬇

Outline

TREATMENT

Appropriate Health Care!!navigator!!

  • CKD, PPID, sepsis/endotoxemia—see chapters listed in See Also
  • Primary PD, DI, DM—mostly outpatient medical treatment

Nursing Care!!navigator!!

  • Primary PD—gradual restriction of water intake (initially to 100 mL/kg/day, which is approximately twice maintenance needs in a temperate climate, followed by a decrease to 75 mL/kg/day after several days) with careful monitoring of body weight and hydration status along with “trial and error” management changes
  • DI—mild water restriction (to 100 mL/kg/day with careful monitoring of body weight and hydration status) and use of medications may help in limiting PU/PD; discontinue water restriction if dehydration or >5% loss of body weight occurs
  • CKD, PPID—see chapters listed in See Also

Activity!!navigator!!

May increase activity to modify behavior of horses with psychogenic PD.

Diet!!navigator!!

  • CKD, PPID—see chapters listed in See Also
  • Increasing the amount of forage in the diet may help to decrease excessive water intake by horses with primary PD
  • Limit availability of supplemental salt to horses with excessive salt consumption

Client Education!!navigator!!

  • Inform clients that provision of adequate fresh water at all times is imperative to prevent dehydration with all pathologic causes of PU/PD
  • Horses with primary PD may need “trial and error” management changes (e.g. increasing turnout time, increasing exercise, provision of a stablemate or other diversions in the stall) along with gradual water restriction
  • DM—inform owners of the indications for euthanasia, i.e. loss of appetite and body condition; progressive weakness

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

PPID

See chapter Pituitary pars intermedia dysfunction.

DI

  • With neurogenic DI, hormone replacement therapy with desmopressin (a potent ADH analog administered as eye drops) has been successful in small-animal patients but has not been described in horses and may be cost prohibitive
  • With nephrogenic DI, replacement hormone therapy is ineffective; the only practical treatment is to restrict sodium and water intake and to administer thiazide diuretics

DM

Insulin replacement therapy in horses with low serum insulin concentrations.

Contraindications!!navigator!!

Gradual water restriction is contraindicated in horses with CKD, PPID, DM, or sepsis/endotoxemia.

Precautions!!navigator!!

  • Perform water restriction with caution in horses with primary PD and DI to avoid significant dehydration
  • Insulin therapy in DM could result in hypoglycemia

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Closely monitor water intake, urine output, USG in all patients with PU/PD to minimize the risk of dehydration; horses with DI are at greatest risk of developing significant dehydration, even during short periods (hours) of water deprivation
  • CKD, PPID——see chapters listed in See Also

Possible Complications!!navigator!!

Moderate to severe dehydration may develop when horses with CKD, DI, or DM are unintentionally deprived of water for short periods.

Expected Course and Prognosis!!navigator!!

  • The course and prognosis depend on the underlying cause. Horses with primary PD or excessive salt consumption generally respond rapidly and favorably with management changes
  • The magnitude of PU/PD with inherited forms of DI may be reduced with mild salt and water restriction and medical therapy. With acquired forms of DI, especially nephrogenic DI from reversible renal disease or drug treatment, PU/PD may last for weeks to months but often may resolve over time
  • Horses with CKD, DI, and DM have a guarded to poor long-term prognosis
  • Horses with PPID can be effectively managed for years with appropriate treatment and management

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Age-Related Factors!!navigator!!

Foals consuming a predominantly milk diet (<2 months old) normally are polyuric. Daily fluid intake may approach 250 mL/kg/day and a USG <1.008 is normal.

Abbreviations!!navigator!!

  • ADH = antidiuretic hormone
  • CKD = chronic kidney disease
  • DI = diabetes insipidus
  • DM = diabetes mellitus
  • PD = polydipsia
  • PPID = pituitary pars intermedia dysfunction
  • PU = polyuria
  • USG = urine specific gravity

Suggested Reading ⬆ ⬇

Mckenzie EC. Polyuria and polydipsia in horses. Vet Clin North Am Equine Pract 2007;23:641–654.

Schott HC. Polyuria and polydipsia. In: Reed SM, Bayly WM, Sellon DC, eds. Equine Internal Medicine, 4e. St. Louis, MO: WB Saunders, 2017:961–966.

Author(s) ⬆ ⬇

Author: Harold C. Schott II

Consulting Editor: Valérie Picandet

Additional Further Reading ⬆

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