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Basics

Basics

Definition

Urinary specific gravity between 1.000 and 1.006

Pathophysiology

The ability to concentrate urine normally (dogs, >1.030; cats, >1.035) depends on a complex interaction between ADH, the protein receptor for ADH on the renal tubule, and a hypertonic renal medullary interstitium; interference with the synthesis, release, or actions of ADH, damage to the renal tubule, and altered tonicity of the medullary interstitium (medullary wash-out) can cause hyposthenuria.

Systems Affected

Depends on the underlying disorder

Signalment

Species

Dog and cat

Breed Predilections

None

Mean Age and Range

None

Predominant Sex

None

Signs

  • Polyuria and polydipsia
  • Urinary incontinence-occasional
  • Other signs depend on the underlying disorder

Causes

Any disorder or drug that interferes with the release or action of ADH, damages the renal tubule, causes medullary wash-out, or causes a primary thirst disorder (see “Differential Diagnosis”).

Diagnosis

Diagnosis

Differential Diagnosis

  • Pyometra
  • Cushing's disease
  • Central diabetes insipidus (little or no ADH produced)
  • Nephrogenic diabetes insipidus (resistance to ADH)
  • Pyelonephritis
  • Hyperthyroidism
  • Hypercalcemia
  • Early renal failure
  • Primary liver disease
  • Hypokalemia
  • Hypoadrenocorticism
  • Primary polydipsia-compulsive water drinking

Laboratory Findings

Drugs That May Alter Laboratory Results

Cortisone, lithium, demeclocycline, methoxyflurane, thiazide diuretics, and intravenous administration of fluids can all lower urine specific gravity into the hyposthenuric range.

Valid if Run in a Human Laboratory?

Yes

CBC/Biochemistry/Urinalysis

  • Low urinary specific gravity (1.000–1.006), other abnormalities may point to the underlying cause.
  • High serum ALP activity suggests hyperadrenocorticism or primary liver disease.
  • High cholesterol common in patients with hyperadrenocorticism.
  • Leukocytosis with a left shift in some patients with pyometra or pyelonephritis.
  • Hyperkalemia and hyponatremia suggest hypoadrenocorticism.
  • Low serum potassium confirms hypokalemia.
  • Inflammatory sediment or bacteriuria consistent with pyelonephritis.
  • Proteinuria common in patients with pyelonephritis, pyometra, and hyperadrenocorticism.

Other Laboratory Tests

ACTH levels to determine the cause of hyperadrenocorticism (i.e., pituitary-dependent vs. adrenal tumor).

Imaging

  • Radiography to assess renal size and shape and to detect calcified adrenal tumor or large uterus.
  • Intravenous pyelogram to help diagnose pyelonephritis.
  • Ultrasonography to assess adrenal size, renal and hepatic size and architecture, and uterine size.
  • MRI or CT scan to assess a pituitary or hypothalamic mass that may be the cause of central diabetes insipidus or hyperadrenocorticism.

Diagnostic Procedures

  • ACTH stimulation test to screen for hyperadrenocorticism and hypoadrenocorticism.
  • Low-dose dexamethasone-suppression test and urine/cortisol creatinine test to screen for hyperadrenocorticism.
  • Serum bile acids to evaluate liver function.
  • Note: dogs with hyperadrenocorticism often have mildly high bile acids.
  • Modified water deprivation test to differentiate diabetes insipidus from psychogenic polydipsia; see Appendix II for test protocol.

Treatment

Treatment

Medications

Medications

Drug(s) Of Choice

Depends on the underlying disorder

Follow-Up

Follow-Up

Patient Monitoring

Urine specific gravity, hydration status, renal function, and electrolytes

Possible Complications

Dehydration

Miscellaneous

Miscellaneous

Associated Conditions

See “Differential Diagnosis”

Zoonotic Potential

None

Abbreviations

  • ACTH = adrenocorticotropic hormone
  • ADH = antidiuretic hormone
  • ALP = alkaline phosphatase
  • CT = computed tomography
  • MRI = magnetic resonance imaging

Suggested Reading

DiBartola SP. Fluid, Electrolyte and Acid-base Disorders in Small Animal Practice, 3rd ed. Philadelphia: Saunders, 2005.

Rose DB, Post T. Clinical Physiology of Acid-base and Electrolyte Disorders, 5th ed. New York: McGraw-Hill, 2000.

Author Melinda Fleming

Consulting Editor Deborah S. Greco

Acknowledgment The author and editors acknowledge the prior contribution of Rhett Nichols.