Polyuria (PU) is defined as urine output greater than 50 mL/kg per day, whereas polydipsia (PD) is defined as water intake greater than 100 mL/kg per day. Clients will often confuse PU/PD with pollakiuria/dysuria (Chapter 32) and/or incontinence (Chapter 34).

The clinical signs of PU and PD are a reflection of responses to regulate fluid volumes necessary to maintain body water homeostasis. Total body water accounts for approximately 60% of the body weight in the adult animal with normal body condition. It is composed of intracellular (approximately 40% of body weight) and extracellular fluid (approximately 20% of body weight). Extracellular fluid is composed of interstitial (approximately 15% of body weight) and intravascular fluid (approximately 5% of body weight). Vascular fluid is the most liable and subject to rapid losses and/or gains with disease processes. It is maintained within a physiologic volume necessary to maintain pressures required to circulate blood from the heart to the tissues and then back to the heart. Fluid or water is retained within the intravascular space by vessel impermeability, in combination with the net of forces that retain vascular fluid (intravascular oncotic pressure) and that promote vascular fluid loss (vascular hydrostatic pressure and extravascular oncotic pressure).

Dehydration is the loss of total body water from all spaces, while hypovolemia or hypervolemia refers to the intravascular space. Body water can shift between the vascular, interstitial, and intracellular spaces as necessary to maintain adequate vascular volume and to preserve intracellular fluid necessary for cellular metabolism (hydration). Excessive water losses from any cause, including the urinary system (PU), result in water being shifted from the interstitial fluid space into the vascular fluid space. In turn, water may be shifted from the intracellular fluid space to replenish the interstitial fluid space. Ultimately, intravascular fluid volume is maintained and hypovolemia is prevented. The body response to offset the loss is to increase water intake (PD) to match water losses (PU). When the vascular water is increased, the interstitial and intracellular fluid that was “borrowed” can eventually be replaced. It follows then that when there is excess intravascular fluid volume from any cause with normal hydration of tissues (interstitial and intracellular spaces are “full”), the fluid excess must be eliminated usually through the urinary system (PU).

Thirst is nothing more than appetite for water. This appetite is governed by the thirst center located in the hypothalamus. Normal stimulants for thirst include increased osmolality, angiotensin II, and vasopressin or antidiuretic hormone (ADH). Increased osmolality, usually with concurrent hypernatremia, is most commonly secondary to excessive sodium ingestion or with free water loss. While ingestion of water containing high concentrations of sodium (alkali water) is unusual, excessive intake of dietary sodium is not. Excessive free water loss often occurs secondary to diarrhea, panting with respiratory disease, and/or polyuria. Decreased renal perfusion secondary to hypotension/hypovolemia, beta-1 sympathetic stimulation, and decreased sodium delivery to the juxtaglomerular apparatus in the kidney activates the renin-angiotensin-aldosterone system. Increase in aldosterone increases sodium and water retention and potassium loss. This coupled with the increased thirst promotes vascular volume expansion. Vascular volume expansion improves renal perfusion and glomerular filtration, promoting a return to fluid homeostasis.

Increased osmolality, volume depletion, and/or angiotensin II cause ADH release from the pituitary. An increase of only 1–2% in serum osmolality induces maximum release of ADH, whereas circulating vascular volume must decrease by 5–10% for a similar ADH response. Water balance in the kidney is regulated primarily by ADH acting on the collecting ducts of the kidneys. ADH binds to receptors on the basolateral membrane of the renal collecting ducts leading to increased permeability to free water and reabsorption. Although ADH is required for water to enter the collecting duct cells, water movement is also dependent on an osmotic gradient within the renal medulla. High urea and sodium chloride concentrations are maintained by the loops of Henle and vasa recta to achieve this osmotic gradient necessary to concentrate the glomerular filtrate (urine) and limit urinary fluid losses. Primary polyuria can be caused by reduced or absent ADH synthesis or release, failure of the collecting ducts to respond to ADH, and/or reduced concentration gradient within the renal medulla.

History and Physical Examination

A thorough history must be obtained to distinguish between PU/PD, dysuria/pollakiuria, and incontinence. To confirm PU/PD, measurement of water intake and/or urine output is required. Clinically, this is not always practical. The simplest method to assess the presence of PU is to measure urine specific gravity. If the urine specific gravity is less than 1.030, the problem of PU/PD should be pursued. The client should be questioned about what is observed during urination. Specific questions regarding frequency, posturing, straining to urinate, and the appearance of urine are important. Polyuric animals would be expected to have normal posture and the ability to consciously void and stop voiding appropriately when outdoors. In contrast, animals with dysuria would strain to urinate and may have discolored (dark or red) urine. Animals with incontinence may void normally when put outdoors; however, at other times unconscious dribbling without posturing will occur. Additional history concerning other clinical signs may assist in determining the cause of the PU/PD. For example, animals with suspected PU/PD that have excessive panting, symmetrical endocrine alopecia, and polyphagia may have hyperadrenocorticism. Once PU/PD is confirmed, a complete drug history should be obtained to identify medications that are expected to cause PU/PD (i.e., furosemide, glucocorticoids, and phenobarbital).