Polyuria and Polydipsia

Chapter 20 Polyuria and Polydipsia


Polyuria (PU) is defined as excessive urine production and is confirmed by demonstrating that daily urine production exceeds the upper limit of normal. In dogs, daily urine volume should normally not exceed approximately 50 mL/kg/day.1 Normal daily urine volume is lower in cats. Frequency of voiding is not incl uded in the definition of PU and may be normal or increased in patients with PU. It is essential that PU not be confused with pollakiuria, the frequent voiding of small quantities of urine.

Polydipsia (PD) is consumption of water in excess of the upper limit of normal daily intake. Normal water intake in dogs is usually less than 60 mL/kg/day with an upper limit of 100 mL/kg/day.1 Because water consumption is easier to measure, it is often used to confirm PD. However, environmental and behavioral factors (e.g., ambient temperature, activity of the animal) may markedly alter water consumption in dogs and should be considered in interpreting these measurements.2 Normal values for water intake are likely substantially less in cats, but a well-defined cutoff value has not been established.

Diagnosis of PU or PD should ideally be confirmed by measuring water intake and/or urine production rate. Because water intake is more easily and accurately measured than urine output, confirmation of PU or PD is often made by measuring daily water intake. Although PD is usually a reliable surrogate for confirming PU or PD, increased water loss via nonurinary pathways (e.g., diarrhea) may be associated with PD absent PU.

Polyuric patients should have reduced urine specific gravity values; therefore, urine concentration is often used as a surrogate for confirming PU. Patients that persistently produce urine less concentrated than expected (i.e., <1.030 for dogs and <1.035 for cats) should be evaluated for a possible pathologic defect in urine-concentrating ability.3 In dogs, urine samples obtained in the morning immediately upon arising are typically the most concentrated and thus provide a more reliable estimate of urine concentrating ability.4 Urinalysis should be performed to determine urine concentration in any patient in which the owner reports increases in water intake or urination, regardless of whether the actual measured water intake exceeds the upper limit for PD. Patients with documented PD that have concentrated urine should be evaluated for nonurinary water losses.

Pathophysiology and Mechanism

General Mechanisms Affecting Water Intake and Urine Volume

Urine concentration and water consumption (thirst) are controlled by interactions between kidneys, pituitary gland, and hypothalamus. Plasma osmolality (primarily sodium concentration) is the primary parameter monitored by this control system. Ingestion of a water load decreases plasma osmolality, while water loss from the body (by any route) increases plasma osmolality. Alterations in plasma osmolality are sensed by receptor cells (i.e., osmoreceptors) in the hypothalamus that affect water intake (via thirst) and excretion (via antidiuretic hormone acting on the kidneys). This system maintains plasma osmolality within a very narrow range.

The normal response to a water load is suppression of antidiuretic hormone (ADH) and thirst. In the absence of ADH, the renal collecting tubules are impermeable to reabsorption of water. In this setting, hypoosmotic tubular fluid leaving the loop of Henle does not equilibrate with renal medullary interstitium resulting in dilute urine, thus allowing elimination of the water load. When PU or PD results from excessive water consumption, plasma osmolality and sodium concentration tend to trend toward the lower end of the normal range.

Correction of a water deficit requires intake and retention of exogenous water. This occurs through increasing thirst and release of ADH in response to an increase in plasma osmolality. Thirst is the primary defense against hyperosmolality. In response to ADH, further loss of water by kidneys is minimized by transient insertion of water-permeable channels (i.e., aquaporin-2) into membranes of renal collecting tubules, thus allowing water to move along its osmotic gradient from lumen of collecting tubules into the hypertonic medullary interstitium producing concentrated urine. When PU or PD results from a defect in urine concentrating ability, plasma osmolality and sodium concentration may trend toward the higher end of the normal range.

In contrast, isoosmotic fluid loss (e.g., many gastrointestinal and urinary fluid losses) typically reduces effective circulating volume without altering plasma osmolality. This decline in effective circulating volume is termed volume depletion rather than dehydration. With volume depletion, both sodium and water retention are needed to correct the volume deficit. Sensors and response system for maintaining effective circulating volume are predominantly focused on modifying renal sodium handling; fluid volume is regulated because water is retained or excreted with sodium.5 Factors active in this process include the renin–angiotensin–aldosterone system, atrial natriuretic peptide (ANP), ADH, and activation of thirst.

General Mechanisms Promoting Primary Polyuria

Ability to conserve or excrete water requires (a) the ability to manufacture and appropriately secrete ADH, (b) maintenance of an appropriately hypertonic renal medulla (i.e., functional renal countercurrent mechanism), and (c) ability of kidneys to respond appropriately to ADH when present. Disruption of any of these processes may cause PU. In addition, an excess of nonreabsorbable solute in the glomerular filtrate and renal tubules (e.g., glucosuria in diabetes mellitus or with mannitol infusion) may also impair the urine-concentrating mechanism. In osmotic diuresis, medullary blood flow is enhanced by an unknown mechanism. This results sequentially in decreased renal papillary osmolality and an elevation in both urine volume and sodium excretion, primarily because of a fall in water reabsorption in the descending limb of the loop of Henle and sodium reabsorption in the ascending limb of the loop of Henle. PU may also occur when the thirst center in the anterior hypothalamus is stimulated resulting in PD. Thus, PU may result from four mechanisms: (a) inadequate production of functional ADH (i.e., central diabetes insipidus), (b) lack of appropriate renal response to ADH (i.e., nephrogenic diabetes insipidus), (c) osmotic diuresis, or (d) primary PD. In the first three of these mechanisms, PU is primary and PD is secondary or compensatory. In the last, PD is primary and the PU occurs as a secondary compensation to eliminate excess water consumed. Combinations of these various mechanisms may occur together in the same patient.

Differential Diagnosis

Table 20-1 summarizes various recognized causes of PU and PD. Many of the causes of PU or PD present with other clinical signs or laboratory abnormalities, which readily facilitate their diagnosis (Table 20-2). In most instances, the cause for PU or PD can be determined from information gathered from history, physical examination, a complete blood count, serum chemistry profile, and urinalysis. The most common causes of PU and PD in dogs include renal disease, hyperadrenocorticism, and diabetes mellitus, whereas the most common causes of PU in cats include renal disease, hyperthyroidism, and diabetes mellitus. Gastrointestinal disease and gastrointestinal leiomyosarcoma have been linked to PU and PD.79 Figure 20-1 is an algorithmic approach to diagnosis.

Table 20-1 Ruleouts for Polyuria and Polydipsia in Dogs and Cats

Ruleout for PU and PD Additional Tests Supporting Diagnosis
Renal disease Glomerular filtration rate (GFR) measurement (creatinine or iothalamate clearance), imaging (ultrasound, radiographs)
Pyelonephritis Urine culture, renal imaging (ultrasound, excretory urography), pyelocentesis (culture, cytology)
Leptospirosis Serology and/or polymerase chain reaction (PCR)
Chronic partial urinary obstruction Urinary tract imaging (ultrasound, contrast radiography)
Renal glucosuria or Fanconi disease Fractional urinary excretion studies (urine amino acids, bicarbonate, glucose, magnesium, phosphate, potassium, sodium)
Primary nephrogenic diabetes insipidus Failure to respond to ADH (usually an exclusion diagnosis, typically a congenital disorder)
Postobstructive diuresis Evidence of recent urinary obstruction, serial declines in serum creatinine and urea nitrogen concentrations
Renal medullary solute washout Seek underlying cause, response to gradual partial water deprivation
Diabetes mellitus Serum fructosamine concentration
Hyperadrenocorticism Adrenocorticotropic hormone (ACTH) response test or low-dose dexamethasone suppression test
Hyperthyroidism (cats) Free thyroxine (T4) by equilibrium dialysis, thyroid scan
Hypoadrenocorticism ACTH response test
Primary hyperaldosteronism Plasma aldosterone, plasma aldosterone-to-renin ratio, oral fludrocortisone suppression test (urinary aldosterone-to-creatinine ratio)
Central diabetes insipidus ADH response test, water-deprivation test, imaging (magnetic resonance imaging [MRI] or computed tomography [CT])
Acromegaly Feline plasma growth hormone concentration (± available), insulin-like growth factor-I concentrations, MRI or CT of the pituitary fossa
Pheochromocytoma Blood pressure, abdominal ultrasound, urine catecholamine concentrations
Hypokalemia (marked)
Hyponatremia (marked)
Blood ionized calcium concentration
Hepatic failure Fasting and postprandial serum bile acids, imaging (ultrasound, radiographs)
Portosystemic shunt Fasting and postprandial serum bile acids, imaging (abdominal ultrasound, portography, rectal scintigraphy)
Leiomyosarcoma Imaging, endoscopy, biopsy
Gastrointestinal disease Imaging, endoscopy, biopsy
Imaging (ultrasound, radiographs)
Pericardial effusion Echocardiogram
Psychogenic (primary) PD Multiple urine specific gravity determinations, ADH response test, water-deprivation testing
Paraneoplastic Imaging (radiographs, ultrasound, CT or MR)
Sudden acquired retinal degeneration syndrome (SARDS)
Retinal examination, electroretinogram

ACTH, Adrenocorticotropic hormone; ADH, anti-diuretic hormone; CT, computerized tomography; GFR, glomerular filtration rate; MRI, magnetic resonance imaging; PCR, polymerase chain reaction; PD, polydipsia; PU, polyuria; SARDS, sudden acquired retinal degeneration syndrome; T4, thyroxine.

Table 20-2 Medical History and Physical Examination Findings Providing Clues to Possible Causes for Polyuria and Polydipsia

Clinical Finding Possible Ruleouts
Weight loss Kidney disease, diabetes mellitus, hyperthyroidism, pyelonephritis, malignancy-induced hypercalcemia, hypoadrenocorticism, hepatic disease, pyometra
Polyphagia Diabetes mellitus, hyperthyroidism, hyperadrenocorticism, acromegaly
Decreased appetite Kidney disease, pyelonephritis, malignancy-induced hypercalcemia, hepatic disease, hypoadrenocorticism
Vomiting Kidney disease, hypoadrenocorticism, pyelonephritis, hepatic failure, hypercalcemia, hypokalemia, hyperthyroidism, diabetes mellitus, consumption of excess water
Malaise and/or weakness Kidney disease, hypoadrenocorticism, pyometra, hypercalcemia, diabetes mellitus, hepatic disease, hypokalemia, hyperadrenocorticism
Behavioral or central nervous system (CNS) signs (seizures, ataxia, stupor, blindness) Hepatic failure, primary PD, central diabetes insipidus, hyperadrenocorticism, acromegaly, sudden acquired retinal degeneration syndrome (SARDS)
Marked PU or PD Primary PD, central diabetes insipidus, congenital nephrogenic diabetes insipidus
Middle-aged female, recent estrus Pyometra
Bilateral alopecia, skin disease Hyperadrenocorticism or other endocrinologic disorders
Abdominal distention Hepatic failure, hyperadrenocorticism, pyometra, nephrotic syndrome, bladder enlargement caused by PU
Hepatomegaly Hyperadrenocorticism, diabetes mellitus, hepatic disease
Small kidneys Chronic or congenital kidney disease
Hypertension, hypertensive retinopathy Chronic kidney disease (CKD), hyperthyroidism, diabetes mellitus, hyperadrenocorticism
Uremic breath, uremic stomatitis Kidney disease
Thyroid or neck mass Hyperthyroidism, hyperparathyroidism, CKD
Heart murmur Hyperthyroidism, CKD, acromegaly
Panting, tachypnea Hyperadrenocorticism, hyperthyroidism, mediastinal mass (lymphoma), pheochromocytoma

CKD, Chronic kidney disease; CNS, central nervous system; PD, polydipsia; PU, polyuria; SARDS, sudden acquired retinal degeneration syndrome.


Figure 20-1 Algorithm demonstrating the diagnostic sequence recommended for establishing the diagnosis of PU and/or PD in dogs and cats. Tables 20-1 and 20-2 provide supplemental information useful in applying the algorithm to patients. ADH, Anti-diuretic hormone; CBC, complete blood count; DI, diabetes insipidus; GFR, glomerular filtration rate; T4, thyroxine.

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Jul 10, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Polyuria and Polydipsia

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