A Clinical Guide to Polyuria and Polydipsia in Cats
By Tara Ghormley, DVM, DACVIM
When a cat begins drinking more water than usual or filling the litter box with an unusual amount of urine, most owners notice quickly. For veterinarians, this paired set of symptoms—polyuria (PU) and polydipsia (PD)—is a clinical red flag. These signs rarely appear without reason. They indicate that the kidneys, hormones, or even other body systems are no longer maintaining normal water balance. Understanding exactly why a cat is experiencing PU/PD requires a deep dive into renal physiology, careful history-taking, and a systematic diagnostic plan.
What Do PU and PD Really Mean?
Polyuria refers to a true increase in urine volume, defined in cats as greater than 50 mL/kg/day. Polydipsia, its frequent companion, means water intake over 100 mL/kg/day. Importantly, PU and PD should not be confused with other urinary tract signs. Frequent small voids (pollakiuria), straining (stranguria), or even incontinence are different problems and point toward lower urinary tract disease rather than systemic water balance disorders.
Normal water intake in cats is not fixed—it shifts depending on the environment, activity level, and diet. Cats eating dry food or fed several times daily may naturally drink more. Recognizing what is “abnormal” requires owners and veterinarians to establish a baseline.
The Physiology of Water Balance
To understand PU/PD, it helps to revisit how healthy cats regulate water.
The thirst center in the hypothalamus is stimulated by two key factors: rising plasma osmolality and falling blood volume. Osmolality is the measure of solute concentration in a solution and in animals it is mainly determined by sodium concentration. When triggered, the hypothalamus not only drives the urge to drink but also stimulates the release of antidiuretic hormone (ADH). ADH binds to cells in the nephron’s collecting ducts, instructing them to reclaim water instead of letting it escape in urine.
The physiology of renal function is imperative to understand urine formation. Plasma is first filtered into Bowman’s capsule within the glomerulus; it is now called the ‘filtrate’. The filtrate becomes concentrated in the descending loop of Henle, where water is pulled back into the interstitium via osmosis. Then, electrolytes are actively reabsorbed in the ascending loop, diluting the filtrate. Finally, in the presence of ADH, the collecting ducts fine-tune the balance by inserting aquaporin channels to reabsorb more water and produce concentrated urine.
For this process to work, several conditions must be met:
A population of functional nephrons.
A strong corticomedullary gradient, maintained by sodium and urea.
Normal ADH production and renal response.
Reasonable water intake that does not overwhelm the system.
When any part of this finely tuned system fails, the result is excessive water loss and compensatory thirst.
Asking the Right Questions
The diagnostic journey starts long before lab tests. Owners should describe not just how often their cat urinates, but how much volume they see, whether blood is present, and if incontinence is noticed. Measuring actual water intake at home, when possible, is extremely helpful.
Diet plays a significant role too. High-sodium or high-protein diets may artificially increase thirst. Cats who switch from a canned diet to kibble may also suddenly increase their water intake. Medications, such as diuretics, are another variable. Interestingly, steroids, notorious for causing PU/PD in dogs, are less likely to cause the same effect in cats.
The Diseases Behind PU/PD
Once abnormal water balance is confirmed, the next step is identifying the cause.
Three diseases account for most feline cases:
Chronic kidney disease (CKD): As nephrons are lost, the remaining units compensate by filtering more plasma, increasing tubular flow. This dilutes the medullary concentration gradient and reduces water reabsorption, resulting in a persistent urine specific gravity (USG) below 1.035.
Hyperthyroidism: Excess thyroid hormone increases renal blood flow, flushing out the medullary gradient (“medullary washout”). It can also directly stimulate thirst. Cats often show systemic signs such as weight loss, hyperactivity, and polyphagia.
Diabetes mellitus: When blood glucose rises above ~270 mg/dL, glucose spills into the filtrate and acts as an osmotic agent, dragging water with it. The kidneys cannot reabsorb enough fluid, even with ADH present, leading to glucosuria and persistently high USG values despite increased urine production and water intake.
Other conditions—ranging from pyelonephritis and liver disease to hypercalcemia, hypokalemia, hyperaldosteronism, and acromegaly—can also impair water balance, either by disrupting ADH signaling or altering the kidney’s concentrating ability. A few rare endocrine diseases, such as Cushing’s or Addison’s disease, occasionally play a role in cats.
Building a Diagnostic Plan
The first rule is to prove that PU/PD is real. This means having owners quantify water intake and evaluating urine output, if possible. A hands-on exam can sometimes reveal scalding or urine retention, indicating lower urinary tract disease or incontinence.
From there, urinalysis provides the first major clue. A single sample with a USG above 1.035 is reassuring: the kidneys can concentrate urine. A consistent pattern of dilute or isosthenuric urine suggests kidney dysfunction, impaired ADH activity, or psychogenic polydipsia.
Isosthenuria (1.008–1.012): May be seen with chronic kidney disease or secondary nephrogenic diabetes insipidus. Examples of causes of secondary nephrogenic diabetes insipidus include hyperthyroidism, pyelonephritis, and hypercalcemia.
Hyposthenuria (<1.008): Indicates a true inability to concentrate, pointing to ADH-related problems or excessive intake such as central diabetes insipidus or psychogenic polydipsia.
Additional tests then narrow the differential list:
CBC and chemistry panels can reveal erythrocytosis, inflammation, diabetes, electrolyte imbalances, or liver disease.
Endocrine testing (T4, fructosamine, ACTH stimulation) helps identify thyroid, diabetic, or adrenal disorders.
Plasma osmolality and abdominal imaging may also be helpful.
For rare cases where central diabetes insipidus is suspected, a desmopressin trial or modified water deprivation test may be performed—these are advanced steps with significant risks and are not commonly needed in cats.
Final Thoughts
Polyuria and polydipsia in cats are common yet complex problems. Most cases trace back to chronic kidney disease, diabetes mellitus, or hyperthyroidism, but a long list of other diseases must remain on the radar. A careful history, systematic diagnostic plan, and clear communication with clients form the backbone of effective case management.
The workup can be frustrating and lengthy, and it is important to manage client expectations. Through a systematic approach, the cause of PU/PD in cats can be identified.