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Polyuria and Polydipsia

Jennifer L. Garcia, DVM, DACVIM (SAIM)
Houston, TX, USA

Physiology of Water Metabolism Etiology/Pathophysiology

Maintenance of water balance is very tightly regu- Polydipsia is defined as a fluid intake >90–100 mL/kg/day
lated between the hypothalamus, pituitary gland, and in dogs and >45 mL/kg/day in cats. Patients may be catego-
kidneys. The main hormone involved in this system is rized as having primary polydipsia with secondary polyu-
arginine vasopressin (AVP) or antidiuretic hormone. ria or primary polyuria with compensatory polydipsia.
AVP is produced in the hypothalamus and stored in Primary polydipsia may arise from psychogenic causes
the posterior pituitary. The primary stimulus for AVP (such as behavioral or environmental issues), liver dis-
release is an increase in plasma osmolality sensed by ease, neurologic disease, fever, and pain. These patients
osmoreceptors in the hypothalamus or a decrease in will often have hyposthenuric urine (1.001–1.005) and
extracellular fluid volume sensed by baroreceptors in have low levels of AVP secondary to excessive thirst and
the aortic sinus, left atrium, and carotid sinuses. decreased osmolality (285–295 mOsm/kg).
Other factors known to stimulate AVP release include Causes of primary polyuria can be divided into those
alterations in blood pressure, hypoglycemia, angio- which result in an osmotic diuresis versus manifestations
tensin II, fever, stress, nausea, pain, exercise, and var- of diabetes insipidus (DI) in which there is AVP insuffi-
ious drugs, hormones, and metabolic disturbances. ciency or insensitivity.
Osmolarity is the concentration of a solutionin Osmotic diuresis occurs when an osmotically active
termsof osmoles of solutes per liter of solution. solute (e.g., glucose or urea) is present in the glomerular
Inveterinary medicine, osmolarity is used to estimate filtrate at a high concentration. This creates a gradient,
the osmolality or tonicityof the extracellular fluid which impedes passive reabsorption of water in the distal
(ECF) space. tubules and results in increased water loss. Illnesses such as
Once released into the circulation, AVP binds to diabetes mellitus (DM), chronic renal failure, primary renal
receptors on the basolateral surface of cells in the glycosuria, and postobstructive diuresis can cause polyuria
renal distal convoluted tubules and collecting ducts. with secondary polydipsia as a result of osmotic diuresis.
This initiates insertion of aqueous (aquaporin) chan- Diabetes insipidus can be further categorized as central
nels into the luminal membrane of these cells. The or nephrogenic. Central DI (CDI) is the less common variant
hypertonicity of the renal medulla can then draw free of this disorder and results from a complete or partial defi-
water from the urine filtrate into the distal portion of ciency in AVP production. Trauma, infection, congenital
the nephron, resulting in concentrated urine. anomalies, neoplasia, or idiopathic processes can cause CDI.
Production of concentrated or dilute urine depends on Nephrogenic DI (NDI) refers to problems at the level
functional kidneys; once greater than two‐thirds of of the kidney, which prevent the patient from being able
nephrons have been lost, the patient will be unable to to concentrate urine appropriately in response to changes
produce concentrated urine despite the effects of AVP. in serum osmolality. These patients are insensitive to the
Decreased concentrating ability may be noted before antidiuretic effects of AVP and excrete higher than nor-
azotemia is evident on routine laboratory tests. mal amounts of urine (Box 8.1).

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical