Page 51 - WSAVA2018
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Complete blood count is often times not rewarding, however it can be used to exclude some differentials (e.g., hyperviscosity) and in some diseases, CBC may increase the suspicion of one differential over the other. For example, stress leukogram and thrombocytosis
may imply hyperadrenocorticism. Serum chemistry is extremely useful and in conjunction with the history, physical examination, CBC and urinalysis findings,
further aid in narrowing down the differential diagnosis list. In animals with diabetes mellitus, hyperglycemia is expected. In diabetes mellitus and hyperadrenocorticism, increased activities of liver and biliary enzymes, hypertriglyceridemia, and hypercholesterolemia are expected. In cats with hyperthyroidism, liver enzymes
are often elevated. In animals with hypoadrenocorticism, electrolyte disorders (hyponatremia and hyperkalemia) are common and may accompany hypoglycemia, hypocholesterolemia and hypercalcemia. In animals with kidney disease, creatinine and urea concentrations are often elevated. In animals with liver failure hypoalbuminemia, hypoglycemia, hyperbilirubinemia, hypocholesterolemia and decreased urea concentration may be identified. Hypercalcemia and hypokalemia can be easily identified as potential causes for PUPD.
Ultrasound examination often completes the initial diagnostic work-up. Hyperthyroid nodules, abnormalities in the adrenal glands, changes in liver and kidneys, should all be assessed.
The above diagnostic work-up is often sufficient to reach a diagnosis, or at least to substantially narrow down the differential diagnosis list. However, in certain occasions, additional tests are required to confirm the diagnosis
(T4, hyperadrenocorticism etc.).
In some animals with PUPD, CBC, serum chemistry, urinalysis and ultrasound examination are completely unremarkable. The main differentials to consider at this point include Stage I CKD (including pyelonephritis), hyperadrenocorticism, diabetes insipidus and primary polydipsia.
Presence of Stage I CKD can be further evaluated by symmetric dimethylarginine (SDMA) measurement,
GFR (endogenous or exogenous creatinine or inulin clearance) and kidney biopsy. Hyperadrenocorticism should be considered even in the absence of any concurrent clinical signs or abnormalities in CBC, serum chemistry, urinalysis and ultrasound. If the index of suspicion for hyperadrenocorticism is low, urine cortisol to creatinine ratio (from voided urine sample obtained by the owners at home) can be used to exclude the disease. However, if the result is abnormally high, this test cannot confirm the diagnosis, and further tests like low dose dexamethasone suppression test and ACTH-stimulation test should be pursued.
In cases where all previously mentioned diagnostic tools were negative, the main remaining differentials include primary polydipsia and diabetes insipidus. In theory, calculated or measured serum osmolality can be used to differentiate these conditions, as in primary polydipsia, the polydipsia is deriving polyuria and
thus serum osmolality is expected to be low, whereas in diabetes insipidus, the polyuria is deriving the polydipsia and thus the serum osmolality is expected to be high. In reality, compensatory mechanisms (i.e., drinking and urination) offset the primary mechanism for PUPD, and serum osmolality remains within
the reference interval. Water deprivation test was previously suggested to differentiate primary polydipsia and diabetes insipidus and further to differentiate central vs. nephrogenic diabetes insipidus. However, this test is not risk free and thus, unless primary polydipsia is highly suspected (young, active dogs),
this test is mostly replaced by an ADH trial. In this test, ADH is administered (orally or to the conjunctival sac) after the owners have quantified and established the daily water consumption. Water quantification should be continued daily after ADH administration. A 50% decrease in water consumption is confirmatory for the diagnosis of CDI. A common mistake is to rely on spot USG to confirm the diagnosis. One has to consider that often times, the change in urine USG on a spot sample may not be very different from the baseline, as the administered ADH is not active throughout the day, and when the serum ADH is low, the urine is quickly dilutes and a large volume of highly diluted urine masks the transient increase in urine USG.
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