The ins and outs of polyuria and polydipsia in veterinary practice - DVM
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The ins and outs of polyuria and polydipsia in veterinary practice
There are many terms used to describe abnormalities in urine production. Here we set out to provide a concise reference for the most common ones you'll encounter in veterinary practice.


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What is polyuria?

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 or solutes, polyuria may be normal (i.e. physiologic or compensatory) or abnormal (i.e. 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.

Let's take a look at the different types of polyuria and how to recognize them.

> Physiologic polyuria. The most common cause of polyuria is physiologic. Physiologic polyuria 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 after ingestion of sufficient quantities of salt to increase thirst, administration of diuretic agents, administration of glucocorticoids (especially in dogs), parenteral administration of fluids, administration of phenytoin (antidiuretic hormone [ADH] inhibition) and administration of synthetic thyroid hormone supplements.

> Pathologic polyuria. On the basis of different pathophysiologic mechanisms, pathologic polyuria may be classified as water diuresis or solute diuresis.

In general, water diuresis is characterized by a urine specific gravity (1.001 to 1.006) and osmolality (50 to 150 mOsm/kg H2O) below that of glomerular filtrate (urine specific gravity = 1.008 to 1.012; osmolality = approximately 300 mOsm/kg H2O). Water diuresis commonly results from insufficient ADH (i.e. central diabetes insipidus), decreased renal response to adequate concentrations of antidiuretic hormone (i.e. renal diabetes insipidus) or excessive water consumption (i.e. pathologic thirst including psychogenic polydipsia).

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) 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).


Table 1: Characteristic urine volumes and urine specific gravity values associated with different types of azotemia in dogs and cats
Disorders associated with pathologic polyuria and solute diuresis include chronic primary renal failure, the diuretic phase of acute renal failure, postobstructive diuresis, diabetes mellitus, hyperadrenocorticism and some hepatic disorders (see Table 1).

Polyuria associated with clinical dehydration (caused by vomiting or diarrhea) indicates that the kidneys are unable to conserve water in spite of the body's need for water. If renal function were normal, physiologic oliguria would be expected to occur as a compensatory response of the kidneys to restore fluid balance. Diseases commonly but not invariably associated with polyuria, vomiting and clinical dehydration include primary renal failure (regardless of cause), diabetic ketoacidosis, some cases of pyometra and some cases of liver disorders.

Although polyuria, polydipsia and dehydration may be associated with central diabetes insipidus, nephrogenic diabetes insipidus, hyperadrenocorticism and primary polydipsia, these diseases are not typically associated with severe vomiting.


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Source: DVM360 MAGAZINE,
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