The ins and outs of polyuria and polydipsia
Jun 01, 2003
Polydipsia defined Polydipsia is defined as increased thirst or greater than normal water consumption. Daily maintenance water requirements for dogs may be calculated from the formula [140 x (body weight in kg.)0.75 ]. Daily maintenance water requirements for cats may be calculated from the formula [80 x (body weight in kg.)0.75]. Normal water consumption usually will not exceed approximately 90 ml/kg/day in dogs, or 45 ml/kg/day in cats. Water consumption of greater than 90 ml/kg/day by dogs or 45 ml/kg/day by cats is evidence of polydipsia.
What volume of urine is normal? Normal urine volume is influenced by several variables. It has been estimated that normal adult dogs in a normal environment will produce approximately 20 to 40 ml of urine per kilogram of body weight per 24 hours (1.0 to 2.0 ml/kg/hour). In one study, normal adult cats produced an average of 28 ml of urine per kilogram of body weight per 24 hours.Normal 24-hour urine volume for kittens has been estimated to range between 5 and 60 ml per kilogram of body weight. Newborn puppies have a comparatively limited ability to concentrate or dilute urine in response to changes in extracellular fluid volume.
Puppies and kittens are predisposed to rapid dehydration as a result of their higher water requirements, their comparatively greater insensible water losses, and their decreased ability to maximally concentrate urine.
How is polyuria defined? Polyuria is defined as the formation and elimination of large quantities of urine. The term diuresis is also defined as formation of abnormally large volumes of urine. Urine volume in excess of 45 ml/kg/day in dogs, and 40 ml/kg/day in cats is consistent with polyuria. Depending on the body's need to conserve or eliminate water and/or solutes, polyuria may be normal (physiologic or compensatory) or abnormal (pathologic). For example, polyuria is an appropriate response to water consumption in excess of need. However, polyuria is inappropriate when dehydration is present. Without knowledge of additional information obtained from the history, physical examination, results of urinalysis, and so on, the clinical significance of polyuria cannot be reliably determined.
Physiologic polyuria The most common cause of polyuria is physiologic polyuria. It usually occurs as a compensatory response to increased fluid intake.
Verification that a patient has physiologic polyuria may require a provocative water deprivation or vasopressin response test.
Pharmacologic polyuria Pharmacologic polyuria may occur: 1) following ingestion of sufficient quantities of salt to increase thirst, 2) following administration of diuretic agents, 3) following administration of glucocorticoids, especially in dogs, 4) following parenteral administration of fluids, 5) following administration of phenytoin (ADH inhibition), and 6) following administration of synthetic thyroid hormone supplements.
Pathologic polyuria On the basis of different pathophysiologic mechanisms, polyuria may be classified as water diuresis or solute diuresis.
In general, water diuresis is characterized by a urine specific gravity (SG = 1.001 to 1.006 ) and osmolality (Osm = 50 to ± 150 mOsm/kg H2O) below that of glomerular filtrate (SG = 1.008 to 1.012; Osm = approximately 300 mOsm/kg H2O).
Water diuresis commonly results from insufficient antidiuretic hormone (central diabetes insipidus), decreased renal response to adequate concentrations of antidiuretic hormone (renal diabetes insipidus) or excessive water consumption (pathologic thirst including psychogenic polydipsia).
In general, solute diuresis is characterized by a urine specific gravity and osmolality equal to or greater than that of glomerular filtrate. Solute diuresis results from excretion of solute in excess of tubular capacity to absorb it (i.e. glucose in diabetes mellitus), impaired tubular reabsorption of one or more solutes (i.e. urea, creatinine, phosphorus and other solutes in primary renal failure), and/or abnormal reduction in medullary solute concentration that impairs the countercurrent system (i.e. decreased renal medullary urea in patients with portovascular shunts and decreased renal medullary sodium in patients with hypoadrenocorticism).