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Primary polydipsia

Primary polydipsia is a disorder characterized by excessive voluntary intake of fluids in the absence of underlying physiological stimuli such as elevated plasma osmolality, resulting in polyuria (urine output exceeding 40-50 mL/kg per 24 hours) and a risk of hyponatremia due to dilution of serum sodium levels. It encompasses two main subtypes: psychogenic polydipsia, often associated with psychiatric conditions, and dipsogenic polydipsia, driven by an abnormal thirst mechanism in the hypothalamus. Unlike diabetes insipidus, where polyuria precedes polydipsia, primary polydipsia originates from the excessive drinking itself, which suppresses antidiuretic hormone (ADH) release and impairs the kidneys' ability to concentrate urine. The condition is most prevalent among individuals with psychiatric disorders, particularly , where it affects up to 18% of inpatients, though it also occurs in those with neurodevelopmental disorders, anxiety, obsessive-compulsive disorder, or even as a habitual behavior in health-conscious individuals without mental illness. Risk factors include severe mental illness, brain injuries, and certain medications that may exacerbate compulsive behaviors, with dipsogenic forms linked to hypothalamic damage or a reset osmostat that lowers the . Epidemiologically, psychogenic polydipsia is more common in psychiatric populations, while dipsogenic cases show a rising trend among women pursuing healthy lifestyles involving high fluid intake. Pathophysiologically, excessive water consumption overwhelms the kidneys' excretory capacity (up to 12-20 liters per day under normal conditions), leading to hypo-osmolar urine and potential if intake exceeds 15-20 liters daily. Clinically, primary polydipsia presents with persistent thirst () and large volumes of dilute urine, often exceeding 3-5 liters per day, alongside symptoms of such as , , , seizures, or in severe cases, and death if serum sodium drops below 120 mEq/L. Complications extend beyond acute to include chronic issues like from repeated electrolyte shifts and potential renal damage from sustained . In psychiatric patients, it is associated with higher morbidity and mortality, with affected individuals experiencing a median age of death around 57 years compared to 68 years in non-polydipsic patients. Diagnosis involves confirming through 24-hour urine collection, assessing serum electrolytes and osmolality (typically low-normal in PP), and distinguishing it from via water deprivation testing or copeptin levels, though the former has only 41% accuracy for PP. primarily relies on fluid restriction to 1-2 liters per day, which can normalize sodium levels but is challenging in non-compliant patients; pharmacological options are limited, with showing promise in psychotic cases, vaptans (vasopressin antagonists) for acute , and cautiously for dipsogenic subtypes. Behavioral s and addressing underlying psychiatric conditions are essential for long-term management, as hinges on adherence and early to prevent life-threatening complications.

Definition and Classification

Definition

Primary polydipsia (PP) is defined as excessive voluntary without underlying physiological stimuli, typically exceeding 3-4 liters per day in adults or 40-50 mL/kg body weight per 24 hours, which results in and hypotonic characterized by dilute urine with low osmolality. This condition encompasses subtypes such as psychogenic polydipsia, often linked to psychiatric disorders, and dipsogenic polydipsia, related to hypothalamic dysregulation. In contrast to (DI), where stems from deficient antidiuretic hormone action or renal response, leading to secondary and fluid intake, PP features primary excessive consumption that drives urinary output and suppresses arginine secretion. Healthy kidneys can excrete up to approximately 12 liters of dilute urine per day in response to such excess intake, thereby mitigating risks like severe unless fluid consumption substantially surpasses this threshold.

Types

Primary polydipsia is broadly classified into psychogenic polydipsia and dipsogenic polydipsia, with additional variants including habitual and iatrogenic forms, distinguished by their underlying behavioral, neurological, or external triggers. Psychogenic polydipsia, the most common subtype accounting for the majority of cases, is characterized by excessive fluid intake driven by psychiatric disorders or compulsive behaviors rather than physiological thirst. It is frequently observed in patients with (affecting 11-20% of those with chronic forms), where it manifests as the psychosis-intermittent hyponatremia-polydipsia syndrome, involving daily intakes of 5-15 liters to alleviate or as a habitual compulsion. This type also occurs in other conditions such as anxiety, , obsessive-compulsive disorder, , and substance use disorders, with features like a reset osmostat for thirst and delayed fluid satiation. Developmental or habitual compulsive drinking without overt psychiatric illness can further contribute, emphasizing behavioral dysregulation over organic causes. Dipsogenic polydipsia arises from primary dysregulation of the thirst center in the , leading to excessive independent of psychiatric factors, often with a lowered osmotic thirst threshold (around 280-285 mOsm/kg compared to the normal ~295 mOsm/kg). It includes idiopathic forms and those secondary to structural damage, such as lesions from granulomatous diseases (e.g., ), infections (e.g., ), vascular issues (e.g., ), or , which lower the osmotic threshold for thirst stimulation. Patients typically exhibit intakes exceeding 3-4 liters per day, resulting in and potential , but without the compulsive elements seen in psychogenic cases. Other variants encompass habitual polydipsia, where individuals consciously overhydrate due to choices, such as health-conscious routines, athletic , or beliefs in benefits, often without underlying . Iatrogenic polydipsia, though less common, results from external influences like medical recommendations for high fluid intake or medications that enhance thirst perception, including certain antidepressants, antipsychotics (e.g., ), or anticholinergics. These forms highlight non-pathologic or induced mechanisms that mimic primary polydipsia but require targeted intervention to prevent complications.

Etiology and Pathophysiology

Causes

Primary polydipsia arises from a variety of etiological factors, often multifactorial in nature, leading to excessive fluid intake without underlying physiological stimuli such as elevated plasma osmolality. Psychiatric conditions represent a major category of causes, particularly in patients with schizophrenia, where primary polydipsia, also known as psychogenic polydipsia, affects up to 20% of inpatients. This association is attributed to compulsive behaviors and altered thirst regulation observed in schizophrenia spectrum disorders. Primary polydipsia also occurs in individuals with intellectual disabilities, including those with moderate to profound levels, where habitual excessive drinking patterns contribute to the condition. Anxiety disorders further predispose patients to this disorder, often linked to psychological stress responses that manifest as increased fluid consumption. Neurological etiologies involve disruptions to central thirst regulation mechanisms, such as hypothalamic lesions resulting from tumors, infiltrative diseases, or . , in particular, can damage the thirst centers in the , leading to dipsogenic forms of primary polydipsia. Other causes include iatrogenic factors from medications, where effects of antipsychotics induce dry mouth and subsequent thirst, while may exacerbate polyuria-polydipsia cycles in susceptible individuals. Nutritional deficiencies play a role in conditions like beer potomania, observed in malnourished patients with chronic excessive beer intake, which limits renal free water excretion and promotes . Idiopathic or habitual patterns, including compulsive water drinking without identifiable psychiatric or neurological basis, also contribute, often seen in otherwise healthy individuals. Risk factors for primary polydipsia, particularly dipsogenic variants, include a predominance, potentially linked to hormonal influences or higher rates of anxiety-related behaviors. Additionally, associations with healthy trends, such as excessive for purported or benefits, have emerged in health-conscious populations.

Primary polydipsia (PP) is characterized by excessive voluntary fluid intake driven by abnormal mechanisms, leading to disruptions in fluid and balance. The primary pathophysiological defect involves dysregulation of the center in the , which fails to appropriately suppress signals in response to hypo-osmolality. This results in persistent water-seeking behavior despite adequate or excessive hydration, overriding normal homeostatic controls. Excessive voluntary fluid intake in PP lowers , appropriately suppressing arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), secretion from the via sensitive osmoreceptors. This results in minimal antidiuretic effects in the renal collecting ducts, producing dilute with osmolality typically below 100 mOsm/kg. The core abnormality is in -regulating pathways, which may involve structural or functional alterations in the , such as a reset osmostat lowering the thirst threshold in dipsogenic forms or dopaminergic/ dysregulation in psychogenic forms. Although the kidneys can excrete large volumes of free water under these conditions, the excessive intake in PP often exceeds the maximum urinary dilution capacity (up to 15-20 L/day), leading to water retention and dilutional hyponatremia. This imbalance is quantified by free water clearance, calculated as: C_{H_2O} = V \times \left(1 - \frac{U_{osm}}{P_{osm}}\right) where V is urine volume, U_{osm} is urine osmolality, and P_{osm} is plasma osmolality. In PP, C_{H_2O} is markedly elevated due to the low U_{osm}, reflecting the kidneys' inability to compensate for the polydipsia-induced water load.

Clinical Presentation

Signs and Symptoms

Primary polydipsia is characterized by an intense sensation of that drives compulsive fluid intake, typically exceeding 3 liters per day and sometimes reaching 5 to 15 liters in severe cases. This excessive , or , is often the presenting complaint, particularly in non-psychotic forms where patients actively seek out fluids due to a perceived need. Accompanying this is , defined as urine output greater than 40 to 50 mL/kg per 24 hours, resulting from the kidneys' attempt to excrete the surplus water load. , or frequent nighttime urination, is also common, disrupting and contributing to daytime . Associated physical signs include from transient fluid retention, with acute increases of more than 5 to 8 kg serving as a clinical indicator of excessive . Patients may exhibit a notable for cold , which can intensify the drinking behavior. These signs reflect the body's response to chronic over, where remains low-normal due to suppressed release. Subtle behavioral indicators often manifest socially, such as constantly carrying bottles or cups and drinking fluids more frequently than peers, often consuming larger volumes in affected psychiatric patients. This habitual preoccupation with can interfere with daily activities and social interactions. While generally benign, unchecked carries a risk of , potentially leading to neurological symptoms if sodium levels drop below 125 mEq/L.

Complications

Primary polydipsia predisposes individuals to due to excessive water intake that exceeds the kidneys' maximal diluting capacity, resulting in dilutional lowering of serum sodium levels. Acute manifests with symptoms such as , , and seizures, potentially progressing to if untreated. , in contrast, is associated with cognitive impairments, including deficits in and executive function. Beyond , severe complications include from rapid osmotic shifts, which can lead to and death. may also occur secondary to hyponatremia-induced cellular swelling and membrane disruption, as reported in case studies of polydipsic patients with significant sodium depletion. Overly rapid correction of hyponatremia carries the risk of osmotic demyelination syndrome, also known as , characterized by demyelination in the and extrapontine regions. Long-term effects of untreated primary polydipsia encompass renal strain, manifested as diminished concentrating ability and potential urinary tract abnormalities that may progress to . Chronic complications also include from recurrent disturbances. In patients with comorbid psychiatric conditions, persistent imbalances can exacerbate overall morbidity, including recurrent hyponatremic episodes and higher mortality, with affected individuals experiencing a age of death around 57 years compared to 68 years in non-polydipsic patients.

Diagnosis

Diagnostic Approach

The diagnostic approach to primary polydipsia begins with a thorough initial evaluation to identify excessive voluntary fluid intake and confirm hypotonic . A detailed history focuses on daily fluid consumption, often exceeding 3-4 liters, which may be linked to psychiatric conditions or habits, alongside assessment of volume (>3 L/24 hours via collection). Laboratory tests include serum sodium, typically <135 mEq/L indicating hyponatremia in chronic cases, and plasma osmolality, which is normal or low; urine osmolality is markedly dilute, often <100 mOsm/kg, reflecting water overload. The water deprivation test (WDT) serves as a key confirmatory step, involving fluid restriction for up to 18 hours while monitoring weight, plasma osmolality, and urine output. In primary polydipsia, urine osmolality rises by >50% from baseline (typically to 300-800 mOsm/kg) due to intact response, with minimal further increase (<9%) after desmopressin administration, distinguishing it from diabetes insipidus where no significant rise occurs. This test has an accuracy of approximately 70-77% but can be nondiagnostic in partial forms due to overlapping results. For challenging cases with overlapping WDT findings, advanced testing involves copeptin measurement, a surrogate for arginine vasopressin. Basal copeptin levels (<10 pmol/L) overlap between primary polydipsia and central diabetes insipidus, necessitating stimulation protocols for differentiation. Hypertonic saline infusion (3% NaCl to achieve serum sodium ≥149 mmol/L) yields copeptin >4.9 pmol/L, confirming primary polydipsia with >95% accuracy; alternatively, infusion (30 g over 30 minutes) with copeptin >3.8 pmol/L after 60 minutes achieves 93% accuracy and is better tolerated. Recent advancements include urea-stimulated copeptin testing to exclude arginine vasopressin deficiency, where post-urea levels >3.5 pmol/L after 120 minutes support primary polydipsia, with 93% , offering a less invasive option with emerging validation. Additionally, a 2025 novel diagnostic score integrates basal parameters ( sodium × osmolality / 100), clinical features (e.g., ≥3 times/night [+30 points], sudden onset [+20 points], >1 L nighttime intake [+30 points], pituitary history [+50 points]), and copeptin >4.9 pmol/L (-50 points), achieving 86% overall accuracy and diagnosing 75% of cases without dynamic testing.

Patient Profiles

Primary polydipsia most commonly manifests in psychiatric patients, particularly those with schizophrenia spectrum disorders, where it affects 6% to 20% of individuals. These patients are often middle-aged males, typically between 40 and 50 years old, with a history of chronic illness and institutionalization. The condition is frequently observed in inpatient settings, contributing to prolonged hospitalizations and complicating care. In contrast, dipsogenic or idiopathic forms of primary polydipsia predominate in individuals without significant psychiatric comorbidity, occurring more frequently in women and those with healthy lifestyle habits. These cases may involve elderly patients or health-conscious adults who habitually consume excessive fluids, potentially driven by trends promoting high water intake for detoxification or cognitive benefits, leading to an observed increase in non-psychiatric presentations. Affected individuals often lack overt psychiatric symptoms and attribute their intake to a persistent sensation of thirst. Pediatric cases of primary polydipsia are rare but can be associated with developmental disorders such as or . Recent reports highlight instances in toddlers, including a 16-month-old female and a 3-year-old , where habitual excessive intake led to imbalances without underlying endocrine .

Treatment and Management

Fluid Restriction

Fluid restriction serves as the primary management strategy for primary polydipsia, aiming to normalize sodium levels by limiting excessive water intake that leads to dilutional . The approach emphasizes gradual reduction in daily fluid consumption to approximately 1-1.5 liters per day, preventing rebound and ensuring patient tolerance while monitoring for resolution of through serial assessments. This controlled limitation helps restore the body's , as unrestricted intake in primary polydipsia often exceeds 3 liters daily, suppressing antidiuretic hormone and impairing urine concentration. In cases of acute, symptomatic secondary to primary polydipsia, immediate intervention with hypertonic 3% saline is indicated to address severe neurological symptoms such as seizures or altered mental status. Infusion rates of 1-2 mL/kg/hour are typically used to achieve an initial rise in sodium of 4-6 mEq/L within the first few hours, with close to avoid overcorrection exceeding 10 mEq/L per 24 hours, which could precipitate osmotic demyelination. Following initial stabilization, fluid restriction is reinstituted to maintain sodium levels, often targeting a gradual increase of no more than 5 mEq/L per treatment session. Implementation of fluid restriction requires inpatient supervision, particularly for patients with underlying psychiatric conditions where adherence is challenging due to intense cues and compulsive behaviors. focuses on recognizing and managing thirst signals without unrestricted access to fluids, often involving structured schedules and environmental controls in hospital settings to facilitate . In psychiatric populations, this strategy may be briefly supported by behavioral techniques to reinforce restriction habits, though long-term success hinges on multidisciplinary oversight.

Behavioral Interventions

Behavioral interventions for primary polydipsia primarily target the psychological and habitual aspects of excessive fluid intake, aiming to modify compulsive behaviors and improve self-awareness of cues. () is a key approach, focusing on identifying and restructuring maladaptive thoughts related to thirst misperception and compulsive drinking habits. Through techniques such as relaxation training, response prevention, and , helps patients recognize triggers for overhydration and develop alternative coping strategies. Small case studies have demonstrated its efficacy, with one report showing sustained reduction in fluid intake and normalization of sodium levels in a patient with chronic polydipsia following an 8-week outpatient program. Monitoring programs form another cornerstone, involving structured tracking of fluid and output to foster accountability and prevent . In institutional settings, staff oversight ensures compliance, often incorporating schedules where positive behaviors, such as adhering to intake limits, are rewarded to encourage change. Self-tracking methods, including log diaries or digital tools for recording consumption, empower patients to monitor their patterns independently, with family or caregivers involved as co-therapists in some cases. A case example illustrated successful intake reduction from 10 liters to 5 liters daily over 6 weeks using a supervised input/output chart. These programs are particularly effective in psychiatric populations when combined with behavioral . Education and counseling emphasize informing patients and families about the risks of excessive fluid intake, such as and its complications, to promote voluntary adherence to management strategies. Sessions typically cover the physiological impacts of and practical self-management techniques, enhancing motivation in compliant individuals. In psychiatric patients who engage actively, educational interventions can reduce compulsive behaviors, though outcomes vary based on underlying factors. Fluid restriction can serve as a brief adjunct to these educational efforts in acute scenarios.

Pharmacological Options

There is no established first-line pharmacological treatment specifically proven for primary polydipsia, with management primarily relying on non-drug approaches for most cases. In patients with underlying psychiatric conditions, such as schizophrenia-associated psychogenic , antipsychotic medications like have shown efficacy in reducing excessive fluid intake and normalizing . For instance, at doses of 300-600 mg daily has been reported to decrease in treatment-refractory schizophrenic patients, potentially through modulation of central mechanisms. Other s, such as , may offer adjunctive benefits in similar contexts but with less consistent evidence. Vaptans, such as , are antagonists that can be used to treat associated with primary polydipsia by promoting aquaresis, the of electrolyte-free , particularly in euvolemic or hypervolemic states. They are effective in psychotic patients with psychogenic polydipsia but require monitoring for rapid sodium correction. Adjunctive pharmacological options include , a dosed at 300-600 mg per day, which induces a reversible nephrogenic insipidus-like state by interfering with hormone action at the renal tubules, thereby promoting free and mitigating risks from overhydration. , a typically administered at 250 mg twice daily, provides mild by inhibiting reabsorption in the , leading to improved and balance in multiple case reports and small series. These agents are used cautiously due to potential side effects, including and with , and or with . Emerging therapies involve (GLP-1) receptor agonists, such as or , which have reduced daily fluid intake by approximately 17-20% and perception in randomized controlled trials of patients with primary polydipsia, possibly via central suppression of appetite and signals. (AVP) analogs, such as , are generally avoided or used with extreme caution due to the risk of exacerbating through enhanced water retention, though low doses may be considered in dipsogenic subtypes to maintain serum osmolality below the threshold for symptomatic relief. As of 2025, no pharmacological agent has received FDA approval specifically for treating primary polydipsia, highlighting the need for individualized risk-benefit assessment in all cases.

Differential Diagnosis

Versus Diabetes Insipidus

Primary polydipsia (PP) and (DI), particularly central DI, present with similar symptoms of and , but they differ fundamentally in underlying , making accurate differentiation essential for appropriate . In PP, excessive voluntary fluid intake drives the condition, suppressing antidiuretic hormone (ADH, also known as arginine vasopressin or AVP) secretion and leading to dilute urine, whereas in central DI, deficient AVP production from the results in uncontrolled water loss and secondary . Biochemically, patients with PP typically exhibit low or normal (often <280 mOsm/kg or sodium <135 mmol/L) due to overhydration, with AVP levels suppressed by the chronic low-osmolar state; however, AVP rises appropriately during water deprivation as osmolality normalizes. In contrast, central DI is characterized by high (>295 mOsm/kg or sodium >145 mmol/L) from free water loss, with low or absent AVP that fails to increase even under osmotic stress. These osmolality and AVP patterns provide initial clues, though direct AVP measurement is rarely used clinically due to assay challenges. The water deprivation test (WDT) remains a cornerstone for differentiation, assessing the kidney's ability to concentrate urine under controlled . In PP, urine typically increases to 600–700 mOsm/kg (range 300–800 mOsm/kg) after 8–18 hours of deprivation, reflecting intact AVP responsiveness and renal concentrating capacity. Conversely, in central DI, urine remains low (<300 mOsm/kg) despite rising plasma osmolality, confirming AVP deficiency; administration of desmopressin then increases urine by >50% in central DI but not in nephrogenic forms. Borderline results (300–800 mOsm/kg) may require further testing to distinguish partial central DI from PP. Clinically, thirst in PP is primary and often psychogenic, strongly associated with psychiatric disorders such as (affecting up to 18% of inpatients), , or intellectual disabilities, where behavioral factors drive fluid intake. In central DI, is secondary and physiological, arising from due to , without inherent psychiatric links but potentially tied to hypothalamic-pituitary pathology like tumors or . PP patients may also show nocturnal less prominently than in DI. Recent advancements, such as measuring copeptin (the C-terminal portion of AVP prohormone, a stable surrogate for AVP), have improved diagnostic precision, especially in ambiguous cases. After hypertonic saline stimulation, a copeptin level >4.9 pmol/L strongly favors PP over central DI, with 96.5% diagnostic accuracy in prospective studies, outperforming the WDT. Basal copeptin >5.6 pmol/L offers 100% specificity for PP, while levels ≤5.6 pmol/L indicate possible AVP deficiency. These tools reduce reliance on prolonged WDT, minimizing risks like dehydration.

Other Conditions

Primary polydipsia (PP) must be differentiated from beer potomania, a condition characterized by severe in individuals with chronic consumption, particularly , coupled with and low dietary solute intake. In beer potomania, the limited availability of solutes such as and electrolytes impairs the kidneys' ability to excrete free water, leading to water retention and even with relatively modest fluid intake; this contrasts with PP, where excessive hypotonic fluid consumption overwhelms normal renal free water excretion, resulting in dilute and potential hyponatremia from water overload. Another key differential is the syndrome of inappropriate antidiuretic hormone secretion (SIADH), which presents with euvolemic due to excessive antidiuretic hormone (ADH) activity, causing water retention and concentrated urine (urine osmolality typically >100 mOsm/kg). Unlike , where chronic overhydration suppresses ADH and produces maximally dilute urine ( <100 mOsm/kg), SIADH features inappropriately elevated ADH levels that prevent urinary dilution despite low osmolality. Conditions involving renal failure or solute diuresis, such as or uncontrolled , can also mimic the polyuria of PP but are distinguished by the presence of an osmotic load driving urine output. In these cases, high concentrations of solutes like or glucose in the create an osmotic , resulting in that is iso- or hypertonic relative to plasma, whereas PP involves pure water with hypotonic lacking significant osmotic particles. A critical exclusion criterion for PP is the response to desmopressin in diagnostic testing; patients with PP exhibit no further urine concentration after desmopressin administration because their ADH secretion is intact and suppressed by habitual overhydration, unlike in central diabetes insipidus where desmopressin induces concentration.

Special Considerations

Non-Psychogenic Forms

Non-psychogenic forms of primary , often termed dipsogenic , arise from disruptions in regulation independent of psychiatric influences, primarily involving defects in hypothalamic that lead to an abnormal sensation of and excessive fluid intake. These defects can result from structural abnormalities in the , such as those caused by , infiltration, , or , which impair the normal osmoreceptor response to . Post-traumatic cases frequently occur following injuries that damage -regulating centers, while idiopathic variants lack an identifiable structural cause and may manifest as a primary dysregulation of mechanisms. This form shows a higher incidence in females, though exact prevalence remains undetermined due to underdiagnosis. Habitual polydipsia represents another non-psychogenic subtype, characterized by excessive water consumption driven by lifestyle or behavioral patterns without underlying psychiatric , such as in health-conscious individuals adhering to programs that promote high fluid intake for purported benefits like or performance enhancement. Iatrogenic causes contribute when medications induce dry mouth or , notably agents that reduce salivary flow, prompting compensatory overdrinking; examples include certain antihypertensives or other drugs with similar side effects. In contrast to psychogenic forms, these habitual or iatrogenic cases often stem from external influences like misguided advice, such as recommendations for increased during illness or exercise. Management of non-psychogenic primary polydipsia emphasizes and targeted interventions over behavioral therapies, which show limited efficacy due to the physiological basis of thirst dysregulation rather than volitional . Fluid restriction remains the cornerstone to prevent , but on balanced is particularly effective for habitual cases, helping to normalize intake without strict enforcement. Unlike psychogenic variants, non-compulsive forms carry a lower risk of severe because intake is more responsive to physiological cues, though monitoring is essential in vulnerable groups. Pharmacological options, such as low-dose , may be considered in select dipsogenic cases to reduce , but evidence is preliminary and not universally recommended. Illustrative cases highlight the clinical diversity: in elderly patients, dry mouth from age-related changes or medications can precipitate habitual overhydration, exacerbating risks like falls from ; one reported instance involved an older adult developing mild from routine high-volume tea consumption to alleviate . Among athletes, compulsive hydration practices during endurance events, such as marathons, have led to in otherwise healthy individuals mistaking for signals, underscoring the need for guideline-based fluid strategies.

In Non-Human Animals

Primary polydipsia, characterized by excessive water intake leading to secondary , is recognized in primarily as a behavioral or psychogenic condition in companion animals. In dogs, it is relatively common, particularly in confined or bored pets, where it manifests as compulsive water drinking often linked to environmental , lack of , or underlying neurological issues. In contrast, primary polydipsia is rare in , with only sporadic case reports documenting it as a psychological without identifiable organic causes. Diagnosis in non-human animals mirrors approaches in humans but requires careful differentiation from organic causes like renal disease or diabetes insipidus. Initial evaluation involves measuring daily water intake exceeding 100 mL/kg in dogs or 45 mL/kg in cats, alongside urine specific gravity consistently below 1.008-1.012, indicating dilute urine. A water deprivation test (WDT) is then performed under veterinary supervision; animals with primary polydipsia typically concentrate urine to a specific gravity above 1.030-1.035 once dehydrated, confirming the absence of antidiuretic hormone deficiency. Concurrent bloodwork, urinalysis, and imaging are essential to rule out renal pathology or other systemic diseases. Treatment focuses on addressing behavioral triggers rather than pharmacological intervention. , such as increased exercise, interactive toys, and social interaction, is the cornerstone for managing psychogenic in , often reducing compulsive drinking by alleviating and . Fluid intake monitoring and gradual restriction may be implemented, while administration, if erroneously used for suspected , proves ineffective and highlights the need for accurate . Species-specific variations are notable; in , psychogenic frequently arises from stabling and , prompting excessive water consumption without physiological deficits, and responds to increased turnout and companionship. Research on primary remains limited in wildlife , with few documented cases and significant gaps in understanding its prevalence or triggers beyond captive settings.

Terminology and Advances

Terminology

The term originates from words poly (many) and dipsa (), referring to excessive or fluid intake. The condition now known as primary was first described in the psychiatric literature in 1938, when Barahal reported a case of in a with , highlighting compulsive fluid consumption leading to . Historically, the disorder was termed psychogenic starting in the mid-20th century, reflecting its initial recognition primarily in patients with psychiatric conditions such as , where behavioral factors drive excessive drinking without underlying physiological thirst mechanisms. This emphasized the psychological origins but limited the scope to contexts. Over time, the broader term primary emerged to encompass both psychogenic forms (driven by or psychiatric issues) and dipsogenic forms (stemming from hypothalamic dysregulation or enhanced thirst perception), avoiding the implication that all cases are purely psychological. Dipsogenic is now recognized as a key subtype within primary . Related terminology includes polydipsia-polyuria syndrome (PPS), which denotes the overarching clinical presentation of excessive thirst and urination, serving as a framework that includes primary polydipsia alongside conditions like . It is important to distinguish primary polydipsia from compulsive water drinking, a phrase sometimes used synonymously but more narrowly applied to habitual or non-pathological overconsumption without the full syndrome of dilutional .

Recent Developments

In 2025, researchers introduced a novel diagnostic score utilizing basal laboratory parameters, such as copeptin levels, sodium, and clinical features like , to differentiate arginine vasopressin (AVP) deficiency from primary polydipsia (PP). This score, derived from two international multicenter prospective studies, achieves a sensitivity exceeding 90% and a high-specificity cutoff with 93% specificity, enabling rapid screening without invasive dynamic testing. Complementing this, the urea-stimulated copeptin test, validated in studies conducted from late 2023 to mid-2024, offers a safer to the deprivation test for distinguishing from AVP deficiency. In this approach, oral administration prompts copeptin release in individuals with intact AVP secretion, as seen in patients, but not in those with AVP deficiency; a copeptin cutoff of 3.5 pmol/L at 120 minutes yields 93% , minimizing risks like . Ongoing clinical trials as of 2025 explore pharmacological interventions, such as GLP-1 analogues, for managing fluid intake in . Additionally, 2024 investigations highlighted genetic behavioral variants, such as those in , contributing to manifestations, suggesting heritable factors in non-psychogenic forms. Early implementation of copeptin-based screening has improved prognosis by facilitating timely behavioral interventions and reducing complications. No novel pharmacological treatments for PP have received regulatory approval by 2025, underscoring the reliance on non-drug management strategies.