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Basics ⬇

Basics

Definition

  • PU-greater than normal urine production (dogs, >45 mL/kg/day; cats, >40 mL/kg/day).
  • PD-greater than normal water consumption (dogs, >90 mL/kg/day; cats, >45 mL/kg/day).

Pathophysiology

  • The volumes of urine produced and water consumed are controlled by interactions between the kidneys, pituitary gland, and hypothalamus. Plasma osmolality (normally determined primarily by serum sodium concentration) is the primary parameter monitored by this control system. Volume receptors within the cardiac atria and aortic arch also influence thirst and urine production. PU may occur when the quantity of functional antidiuretic hormone synthesized in the hypothalamus or released from the posterior pituitary is limited, or when the kidneys fail to respond normally to ADH. PD occurs when the thirst center in the anterior hypothalamus is stimulated.
  • In most patients, PD maintains hydration (as normal tonicity) as a compensatory response to PU. Patients' plasma becomes relatively hypertonic and activates thirst mechanisms. Occasionally PD is the primary process and PU is the compensatory response. In this case, the patient's plasma becomes relatively hypotonic because of excessive water intake, ADH secretion is reduced, resulting in PU.

Systems Affected

  • Urologic-full bladder
  • Cardiovascular-circulating volume
  • Endocrine/Metabolic-pituitary gland, hypothalamus play a role in compensation to PU or PD

Signalment

  • Dog and cat.
  • Congenital diseases in many breeds (e.g., central diabetes insipidus, nephrogenic diabetes insipidus, portal-vascular anomalies, certain renal diseases).
  • Hypoadrenocorticism,some causes of primary PD predominantly affect young dogs.
  • Renal failure, hyperadrenocorticism, hyperthyroidism, neoplastic disorders affecting the pituitary and hypothalamus predominantly affect middle-aged and older dogs and cats.

Causes

  • Primary PU due to impaired renal response to ADH-renal failure, HAC (dogs), hyperthyroidism (cats), pyelonephritis, leptospirosis, pyometra, hepatic failure, hypercalcemia, hypokalemia, renal medullary solute washout, dietary protein restriction, drugs, congenital NDI.
  • Primary PU caused by osmotic diuresis-diabetes mellitus, primary renal glucosuria, post-obstructive diuresis, some diuretics (e.g., mannitol and furosemide), ingestion or administration of large quantities of solute (e.g., sodium chloride or glucose), and hypersomatotropism.
  • Primary PU due to ADH deficiency-idiopathic, traumatic, neoplastic, or congenital CDI; some drugs (e.g., alcohol and phenytoin).
  • Primary PD-behavioral, pyrexia, pain, organic disease of the anterior hypothalamic thirst center of neoplastic, traumatic, or inflammatory origin.

Risk Factors

  • Renal, liver and/or endocrine disease
  • Administration of diuretics, corticosteroids, anticonvulsants
  • Low-protein diets
  • Low purine u/d?

Diagnosis ⬆ ⬇

Diagnosis

Differential Diagnosis

Differentiating Similar Signs

  • Differentiate PU from abnormal increase frequency of urination (pollakiuria). Pollakiuria: often associated with dysuria, stranguria, hematuria. Patients with PU void large quantities of urine; patients with pollakiuria frequently void small quantities of urine. Confirm PU/PD by measuring 24-hour water intake and urine output (3- to 5-day collection period preferred).
  • Alternatively, urinary specific gravity measurement may provide evidence of adequate urine concentrating ability (dogs, >1.030; cats, >1.035), ruling-out persistent PU/PD.

Differentiating Causes

  • Renal failure, HAC, and DM (dogs). Renal failure, hyperthyroidism, DM: (cats).
  • If associated with progressive weight loss-consider renal failure, DM, hyperthyroidism, hepatic failure, pyometra, pyelonephritis, hypoadrenocorticism, malignancy-induced hypercalcemia.
  • If associated with decreased appetite-consider kidney disease, pyelonephritis, malignancy-induced hypercalcemia, hepatic disease, hypoadrenocorticism.
  • If associated with polyphagia-consider DM, hyperthyroidism, HAC, acromegaly.
  • If associated with bilateral alopecia orother cutaneous problems-consider HAC, endocrinologic disorders.
  • If associated with uremic breath and stomatitis-consider advanced kidney disease.
  • If associated with vomiting-consider kidney disease, hypoadrenocorticism, pyelonephritis, hepatic failure, hypercalcemia, hypokalemia, hyperthyroidism, DM.
  • If associated with malaise and/or weakness-kidney disease, hypoadrenocorticism, pyometra, hypercalcemia, DM, hepatic disease, hypokalemia, HAC.
  • If associated with palpable thyroid nodule-consider hyperthyroidism.
  • If associated with hypertensive retinopathy-consider renal failure, hyperthyroidism, DM, HAC.
  • If associated with recent estrus (previous 2 months) in a middle-aged intact female-consider pyometra.
  • If associated with abdominal distention-consider hepatic failure, HAC, pyometra, nephrotic syndrome.
  • If associated with lymphadenopathy, anal sac mass or other neoplastic process-consider hypercalcemia of malignancy.
  • If associated with behavioral or neurologic disorder-consider hepatic failure, primary PD, CDI.
  • If associated with marked PD (patients almost continuously seek and consume water)-consider primary PD, CDI, NDI.
  • If patient is on medication, consider drug induced (steroids, diuretics, anticonvulsants) PU/PD.
  • If patient is consuming a urolith prevention/dissolution or high salt diet, consider diet-induced PU/PD.
  • Key point: PU/PD may be the first sign of disease with many conditions.

CBC/Biochemistry/Urinalysis

  • Urinalysis is useful to confirm PU, discriminate water diuresis from solute diuresis, and identify UTI.
  • Serum sodium concentration or osmolality may help differentiate primary PU from primary PD. Measuring serum osmolality is preferred; calculated serum osmolality is not an acceptable alternative.
  • Relative hypernatremia or high serum osmolarity suggests primary PU (values typically at or exceed the high end of normal range).
  • Hyponatremia or low serum osmolarity suggests primary PD (values typically at or below normal range), except in animals with hypoadrenocorticism, which have hyponatremia and primary PU.
  • Azotemia is typical of renal causes for PU/PD, but may also indicate dehydration resulting from inadequate compensatory PD.
  • Unexpectedly low BUN concentrations suggest hepatic failure.
  • With high hepatic enzymes, consider HAC (especially when value for ALP exceeds ALT), hyperthyroidism, hepatic failure, pyometra, DM. Administration of some drugs that promote PU/PD (e.g., anticonvulsants and corticosteroids) also may elevate hepatic enzymes.
  • Persistent hyperglycemia is consistent with DM.
  • Hyperkalemia, particularly if associated with hyponatremia, suggests hypoadrenocorticism or therapy with potassium-sparing diuretics.
  • Hypercalcemia induces PU only when it results from increased ionized calcium (not protein-bound calcium) concentration.
  • Hypercalcemia and hypokalemia can cause, or occur in association with, other diseases that cause PU/PD.
  • Hypoalbuminemia supports renal or hepatic causes of PU/PD.
  • Neutrophilia is consistent with pyelonephritis, pyometra, HAC, corticosteroid administration.
  • USG values 1.001- 1.003 suggest primary PD, CDI, congenital NDI.
  • Glucosuria supports a diagnosis of DM or renal glucosuria.
  • Pyuria, white blood cell casts, and/or bacteriuria should prompt consideration of pyelonephritis.

Other Laboratory Tests

  • ACTH stimulation or dexamethasone suppression tests rule out HAC in middle-aged to older dogs.
  • Thyroxine concentration to rule out hyperthyroidism in middle-aged to old cats.
  • Bile acids (fasting and postprandial) to rule out portosystemic shunt or hepatic failure.
  • Urine culture-chronic pyelonephritis cannot be conclusively ruled-out by absence of pyuria or bacteriuria.
  • Cytologic examination of lymph node aspirate may provide evidence of lymphoma, which induces PU by hypercalcemic nephrotoxicity or direct infiltration of renal tissues.
  • Paired Leptospira titer to rule out leptospirosis.
  • ADH response test to rule-out CDI.
  • Water deprivation testing (to assess ability to make and respond to ADH) is controversial due to humane considerations; use selectively.

Imaging

Abdominal survey radiography, ultrasonography: may provide evidence of renal (e.g., primary renal diseases, urinary obstruction), hepatic (e.g., microhepatica, portal vascular anomalies, hepatic infiltrate), adrenal (e.g., adrenal mass or bilateral adrenal hypertrophy suggesting HAC), or uterine (e.g., pyometra) disorders that can contribute to PU/PD.

Diagnostic Procedures

Modified Water Deprivation with ADH Response Test (see Appendix II)

  • Differentiates CDI from primary PD and NDI. Rule out other causes for PU/PD before performing this test. Controversial, some suggest omitting water deprivation and proceeding directly to ADH administration to rule in CDI. Administration of ADH to patients with primary PD may be dangerous.
  • Useful for patients with marked PU/PD and hyposthenuria.
  • Contraindicated in dehydrated and azotemic patients, but ADH response testing may be performed safely in these patients.
  • Patients that concentrate urine adequately in response to water deprivation have adequate ADH production and renal response to ADH. If other causes have been ruled out, primary PD is presumed to be present.
  • Failure to concentrate urine adequately in response to properly designed water deprivation tests, but further concentrate their urine in response to administration of exogenous ADH = CDI.
  • Failure to concentrate urine adequately in response to water deprivation and also failure to further concentrate urine in response to administration of exogenous ADH = NDI.

Treatment ⬆ ⬇

Treatment

Client Education

Do not withhold water from patients with PU because potentially dangerous dehydration may result.

Medications ⬆ ⬇

Medications

Drug(s) Of Choice

Varies with underlying cause

Contraindications

Do not administer ADH (or any of its synthetic analogs, such as DDAVP) to patients with primary PD because of the risk of inducing water intoxication.

Precautions

Until renal and hepatic failure have been excluded as potential causes for PU/PD, use caution in administering any drug eliminated via these pathways.

Follow-Up ⬆ ⬇

Follow-Up

Patient Monitoring

  • Hydration status-clinical assessment of hydration, serial evaluation of body weight.
  • Fluid intake and urine output provide a useful baseline for assessing adequacy of hydration therapy.

Possible Complications

Dehydration, hypovolemic shock, hypernatremia

Miscellaneous ⬆

Miscellaneous

Associated Conditions

  • Bacterial UTI.
  • Urinary incontinence may develop in dogs with concurrent urethral sphincter dysfunction, presumably because of increased bladder filling associated with PD.

Abbreviations

  • ACTH = adrenocorticotropic hormone
  • ADH = antidiuretic hormone
  • CDI = central diabetes insipidus
  • CRF = chronic renal failure
  • DDAVP = trademark for preparation of vasopressin
  • DM = diabetes mellitus
  • HAC = hyperadrenocorticism
  • NDI = nephrogenic diabetes insipidus
  • PU/PD = polyuria/polydipsia
  • UTI = urinary tract infection

Author David J. Polzin

Consulting Editor Carl A. Osborne

Client Education Handout Available Online