Dogs and cats frequently present for signs related to the urinary tract. These signs may be due to inappropriate urination
(house soiling or urinary incontinence) or may relate to the act of voiding itself. Voiding disorders include abnormalities
in frequency, duration and volume of urine produced. Polyuria refers to an increase in the amount of urine produced (> 50
ml/kg/day). It is difficult to impossible to discuss polyuria without also discussing polydipsia, or increased water consumption.
Polydipsia is defined as water consumption greater than 100 ml/kg/day in the dog and cat. These two disorders occur together
in most instances. Depending on the etiology you might see a primary polydipsia with a secondary polyuria or a primary polyuria
with a secondary polydipsia.
Urinary water losses are regulated by vasopressin and the kidneys ability to respond to this hormone. Central and peripheral
osmoreceptors and baroreceptors respond to increases in plasma osmolality (primarily sodium) and decreases in blood pressure
by stimulating vasopressin release and thirst. Vasopressin then acts on the kidneys by inserting water channels into the
distal tubules and collecting ducts of the nephron. The osmotic pull from the renal medullary interstitium then pulls water
out of the tubules producing a more concentrated urine. Activation of the renin-angiotensin-aldosterone system also plays
a lesser role. The kidneys sense a decrease in blood volume and produce renin which results in the eventual production of
angiotensin II. Angiotensin II, in addition to being a potent vasoconstrictor, also stimulates the thirst center and vasopressin
release. It is now easy to see how a decrease in production or renal responsiveness to vasopressin as well as changes in
the renal tubular:medullary gradient can lead to polyuria.
Causes of primary & secondary polyuria
Disorders that produce a primary polyuria cause an initial increase in urine production most often accompanied by an increase
in water consumption. An osmotic diuresis can cause a primary polyuria by increasing the amount of solutes in the urine.
This increase in tubular solute concentration competes with the medullary solute concentration for water. More common disorders
resulting in high urine solutes include chronic kidney disease, diabetes mellitus, diabetic ketoacidosis, and relief of a
urinary tract obstruction. Less common causes of increased solutes are mannitol administration and primary renal glycosuria.
Disorders that interfere with the renal tubular response to vasopressin (antidiuretic hormone) also cause polyuria. Common
disorders include excess glucocorticoids (exogenous or endogenous), hyperthyroidism, hypercalcemia, liver disease, pyelonephritis,
hypoadrenocorticism, septicemia, Escherichia coli infection, and pyometra. Less common disorders include primary hyperaldosteronism, hypokalemia, acromegaly, polycythemia,
central diabetes insipidus, and primary nephrogenic diabetes insipidus.
Additional causes of polyuria include loss of a functional medullary gradient which can occur as a result of any of the disorders
that causes polyuria and polydipsia as well as with fluid administration.
Disorders that cause an initial polydipsia and secondary polyuria include excess glucocorticoids (decrease vasopressin rlease)
and psychogenic polydipsia. Hepatic insufficiency may cause a primary polydipsia as well.
Causes of polyuria and polydipsia
o Diuretics (loop, thiazide)
o Diabetes mellitus
o Central diabetes insipidus
Urinary tract disorders
o Chronic kidney disease
o Urinary tract obstruction
o Primary renal glycosuria
o Primary nephrogenic diabetes insipidus
o Escherichia coli
o Hepatic disease
o Psychogenic polydipsia
o Diet – low protein