Diagnostic Approach to Polyuria and Polydipsia

Differentiating between the causes of polyuria and polydipsia (PU/PD) is relatively easy when the different disorders are manifested in their classic forms. For example, polyuria that develops after a known head trauma, continues after water restriction and decreases after AVP administration does not require additional tests to justify the diagnosis of central diabetes insipidus. A diagnosis of congenital nephrogenic diabetes insipidus is equally clear if polyuria occurs in a young animal with similarly affected litter mates that have normal screening laboratory tests (including renal function), negative urine cultures and whose polyuria fails to respond to fluid restriction or administration of AVP analogues (e.g. desmopressin).

Often, however, the clinical setting is of minimal help in making a diagnosis and it is then necessary to perform more detailed diagnostic tests. The initial information gathered should allow the inclusion or exclusion of the many common medical disorders associated with polyuria and polydipsia before a diagnostic work-up for the less common disorders of central diabetes insipidus, primary nephrogenic diabetes insipidus or psychogenic polydipsia is embarked upon.

Measurement of water consumption
The first step in any suspected case of polyuria and polydipsia is to establish that the problem actually exists, preferably by a combination of history, random urine SG determinations and, if necessary, home measurement of water consumption over several days.

If the daily water intake is found to be normal or if a random urine SG determination is >1.035, additional history should be obtained to rule out other urinary tract disorders (such as urinary incontinence or dysuria) that commonly are confused with polyuria. If, however, random urine SG are consistently <1.030 in dogs and <1.035 in cats, and daily water intake is >100 ml/kg for dogs and 45 ml/kg for cats, polyuria and polydipsia are indeed present and a diagnostic work-up to determine the cause is warranted.

Minimum clinicopathological data
Once a problem of water balance is confirmed, a practical diagnostic approach is to first rule out the more common causes of polyuria and polydipsia in dogs and cats. Recommended initial diagnostic tests include:

• Complete blood cell count (CBC)
  
• Serum biochemical profile with electrolytes
  
• Serum total thyroxine (T4) determination in middle-aged to older cats

A careful evaluation of this initial database, together with the history and results of physical examination, usually provides the diagnosis immediately (e.g. overt renal failure, hyperthyroidism or diabetes mellitus) or offers clues to as to the underlying cause of the polyuria and polydipsia (see Table below). For example, dogs with hyperadrenocorticism commonly have a stress leucogram (i.e. neutrophilia, lymphopenia and eosinopenia). Over 90% of dogs with hyperadrenocorticism also have high alkaline phosphatase (ALP) activity, whereas over half have hypercholesterolaemia.

In contrast, physical examination findings and routine blood work are generally unremarkable in animals with less common causes of polyuria and polydipsia such as central diabetes insipidus, primary nephrogenic diabetes insipidus and psychogenic polydipsia. When abnormalities are present, they are usually secondary to dehydration caused by water restriction by the owner. Such abnormalities may include a slightly increased packed cell volume (PCV) or hypernatraemia.

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Initial work-up for polyuria and polydipsia in dogs and cats.

Signalment and history

• Age, breed and sex
  
• Reproductive history (intact female?)
  
• Changes in diet or environment?
  
• Overall general health (weight loss or gain, lethargy, vomiting or diarrhoea?)
  
• Appetite normal, increased or decreased?
  
• Drug administration (glucocorticoids, anticonvulsants, diuretics?)

Physical examination

• Kidneys small or misshapen? (chronic renal disease)
  
• Kidneys large? (pyelonephritis, lymphosarcoma)
  
• Hepatomegaly? (hyperadrenocorticism, diabetes mellitus)
  
• Peripheral lymphadenopathy? (lymphosarcoma with hypercalcaemia)
  
• Perianal mass? (anal sac adenocarcinoma with hypercalcaemia)
  
• Vaginal discharge? (pyometra)
  
• Alopecia? Pot belly? (hyperadrenocorticism)
  
• Thyroid mass? (hyperthyroidism)

Complete blood count (CBC), serum biochemical profile and electrolytes, serum thyroxine

• High urea or creatinine? (renal failure)
  
• Hyperglycaemia? (diabetes mellitus)
  
• High alkaline phosphatase activity (hyperadrenocorticism)
  
• Hypercholesterolaemia? (hyperadrenocorticism)
  
• Hypercalcaemia?
  
• Hypokalaemia?
  
• High thyroxine? (hyperthyroidism)

Complete urinalysis and urine culture

• Low urine specific gravity (confirms and defines polyuria)
  
• Proteinuria? (hyperadrenocorticism, pyometra, pyelonephritis, glomerulonephritis)
  
• Glucosuria +/- ketonuria? (Diabetes mellitus)
  
• Active urine sediment? (infection, pyelonephritis)
  
• Positive bacterial culture? (infection, pyelonephritis)

Abdominal radiography or ultrasonography

• Small kidneys with ill-defined renal or irregular border (renal failure)
  
• Increased cortical echogenicity, indistinct corticomedullary junction (renal failure)
  
• Dilated renal pelvis (pyelonephritis)

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Our next blog post we will continue discussing the diagnostic approach to PU/PD, concentrating on the urine's specific gravity.