25/5/2017 Nocturia: Clinical presentation, diagnosis, and treatment ­ UpToDate

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Nocturia: Clinical presentation, diagnosis, and treatment

Author: Theodore M Johnson, MD, MPH

Section Editor: Michael P O'Leary, MD, MPH
Deputy Editor: Howard Libman, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2017. | This topic last updated: Nov 16, 2016.

INTRODUCTION — Nocturia, a common symptom, is defined as waking at night to void, where each
micturition is preceded and followed by sleep [1]. Although by definition even a single episode of awakening to
urinate is nocturia, epidemiological evidence and expert clinical opinion both suggest nocturia is likely clinically
meaningful if a patient voids two or more times nightly [2]. Patients themselves are more likely to consult a
provider about nocturia if they have three or more episodes [3]. New­onset adult nocturnal urinary
incontinence or nighttime bed­wetting (enuresis) is rare and distinct from nocturia and likely requires a
different approach focusing on sleep problems or urinary obstruction [4,5].

Nocturia is a source of significant bother for some patients [6]. Nocturia is one of the most distressing
symptoms in older men with benign prostatic hyperplasia (BPH) [7] and is the lower urinary tract symptom
most strongly associated with poor quality of life ratings [8]. Patients report nocturia as a leading cause of
sleep disturbance, affecting both sleep onset and maintenance [9]. Nocturia is associated with increased rates
of depression [10], work absenteeism [11], lower self­rated physical and mental health [12], congestive heart
failure [13], and increased all­cause mortality [14]. In the very old, nocturia is associated with higher rates of
accidental falls [15­17] and fractures [18,19].

Because nocturia is associated with a variety of clinical syndromes and disorders [20], the diagnostic
approach is often challenging, and treatment may result in only small improvement [21].

This topic will discuss the clinical presentation, diagnosis, and treatment of nocturia in adults. Detailed
discussions of some conditions that cause or are associated with nocturia are presented separately. (See
"Diagnosis of polyuria and diabetes insipidus" and "Clinical manifestations and diagnostic evaluation of benign
prostatic hyperplasia" and "Evaluation of women with urinary incontinence".)

EPIDEMIOLOGY — The prevalence of nocturia is higher with increasing age [12,22­25]. Occasional nocturia
is present in 50 percent of men and women aged 50 to 59 years. Among 18­ to 49­year­olds, more women
than men have nocturia; the sex ratio reverses after 60 years of age, with prevalence greater in men than
women [22]. The prevalence of twice nightly or greater nocturia among men between 70 and 79 is nearly 50
percent [22].

Many women with nocturia also have other urinary tract symptoms (eg, overactive bladder syndrome or
polyuria) [25,26]. However, isolated nocturia without daytime voiding symptoms is also possible. In a cross­
sectional study of over 2000 women aged 40 or older, 40 percent of women who had nocturia had no other
urinary tract symptoms [27]. While pregnant women commonly have nocturia, it nearly always resolves by
three months postpartum [28]. (See "Renal and urinary tract physiology in normal pregnancy", section on
'Frequency and nocturia'.)

Most studies indicate that the prevalence of nocturia is higher in non­Hispanic black men and women, with
Hispanic men and women having an intermediate prevalence compared with non­Hispanic whites [27,29­32].
Higher rates of nocturia in black men and women do not appear to be due to socioeconomic factors [29,30].

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In a group of men aged 50 to 70 followed longitudinally, the risk for developing nocturia was highest in 70­
year­olds and lowest for the 50­year­olds [33]. Every year, approximately 10 percent more men started to void
during the night. Also, older men were much less likely to have a remission of their nocturia when compared
with the younger men. Fluctuations in the symptom make it difficult to provide a reliable incident rate.

Risk factors for nocturia include obesity, hypertension, diuretic usage, snoring, restless leg syndrome, benign
prostatic hyperplasia (BPH), prostate cancer, antidepressant usage, coronary artery disease, congestive
heart failure, and diabetes [12,34,35]. Physical activity has been associated with decreased nocturia [36].
Although nocturia has been associated with increased mortality (15­year survival rates of 76.5 and 84.8
percent for individuals with and without nocturia, respectively), this association is not confirmed by multivariate
analysis correcting for hypertension, diabetes, chronic pulmonary disease, cardiac symptoms, smoking, and
age [37].

CLINICAL PRESENTATION — Patients may initiate a discussion of their sleep being interrupted by nighttime
voiding, or the clinician might learn of nocturia during a review of symptoms. Clinicians should specifically
question about "waking at night to urinate" (or "to pee," "to void," or "to make water") since nearly one­half of
patients do not correctly interpret the term "nocturia" [38]. Occasionally, nocturia can be an indicator of
worsening clinical status of an underlying disease, such as chronic kidney disease [39], lithium toxicity [40],
diabetes mellitus, or congestive heart failure. The most important reason to diagnose nocturia, however, is to
address symptoms and minimize its negative impact on quality of life [41].

Nocturia is insidious in its onset. Few patients present with an abrupt onset of three to four episodes of
nocturia nightly; most individuals describe progressing from having an episode occasionally to having one or
more episodes nightly. Additionally, nocturia has a varied night­to­night occurrence [33]. The number of
episodes of nocturia that are reported by a given individual over time fluctuate significantly as well. In a study
that looked at the reported frequency of nocturia in men with lower urinary tract symptoms who were receiving
placebo as part of a randomized trial, nocturia regression varied between 2 and 33 percent, while nocturia
progression varied between 8 and 54 percent [42]. For some patients, this unpredictability represents another
loss of control in the process of aging [43] and makes it difficult to predict how much sleep a patient can
expect in any given night [44].

It is more valuable to quantify and understand how much distress nocturia causes the patient than to focus on
obtaining a precise count of nightly episodes [45]. While frequency of episodes and "bother" from nocturia are
linked, one study of men with BPH found that the number of nightly nocturia episodes explained only 25
percent of the variance in reported bother. Other factors, such as difficulty returning to sleep following
nighttime awakening, and degree of morning fatigue, contribute to the impact of nocturia [46].

PATHOPHYSIOLOGY — Nocturia can be attributed to any disorder or condition that causes one of the
following (table 1) [47,48]:

● Low­volume bladder void

● Increased volume of nighttime urinary output
● Sleep disturbance

A longitudinal study of 1688 men aged 50 to 78 years found the following factors associated with an increased
prevalence of nocturia: age, maximum voided volume, 24­hour polyuria, nocturnal polyuria, and lower urinary
tract symptoms [49]. In a study of 41 male patients (mean age 72.5 years) with two or more nocturnal
micturitions, the following etiologies were found: nocturnal polyuria 83 percent; low bladder volume capacity
58 percent; bladder outlet obstruction 44 percent; sleep apnea 5 percent [50]. A study of 845 patients with
symptoms of overactive bladder and nocturia found that younger patients (<50 years) were more likely to
have low bladder capacity, and older patients (>70 years) more likely to have increased nocturnal urine
output, based on data from a seven­day voiding diary [51].

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For many patients with nocturia, it is likely that multiple conditions coexist and lead to symptoms. As an
example, a study of 55 patients evaluating comorbid illness found that male patients (mean age 67 years) had
an average of 4.5 medical conditions likely to be related to nocturia [52].

Low­volume bladder voids — Low­volume voids may be due to either reduced bladder capacity or impaired
bladder function. The two most common causes of low­volume bladder voids are an overactive bladder and
bladder outlet obstruction, often related to benign prostatic hypertrophy (BPH).

Increased age has been associated with reduced bladder volume; it is unclear if this is due to age­related
changes in the bladder or to the high prevalence of detrusor hyperactivity in the older population [53]. Since
so many older adults have detrusor hyperactivity, it often appears that aging is associated with small­volume
voids (since this is a result from detrusor hyperactivity). When the separate effects of age and bladder
pathophysiology are carefully teased apart, older women without detrusor hyperactivity appear to have normal
bladder capacity [54]. Increased age is also associated with increased prevalence of BPH. (See
"Epidemiology and pathogenesis of benign prostatic hyperplasia".)

Increased nighttime urinary volume — An increase in urinary volume at night may be due to an increase in
the total 24­hour urine output, or to a higher percentage of the total daily urine output being excreted at night.

Nocturnal polyuria — The normal pattern of urination is a decrease in nighttime, relative to daytime, urine
output. Overproduction of urine at night, with a normal 24­hour urine output, is called nocturnal polyuria [55].
The definition of nocturnal polyuria is age­dependent, and for older adults (>65 years) has been defined as
nocturnal urine volume greater than 33 percent of the 24­hour urine volume [20].

● Role of arginine vasopressin – Nocturnal polyuria may be due to age­related changes in the secretion
and action of arginine vasopressin (AVP) [56,57]. AVP, a peptide hormone secreted by the
neurohypophyseal system, is released when plasma osmolality is increased or blood pressure decreased
(as seen with orthostasis, vasodilation, or significant blood loss). AVP targets receptors in the renal distal
tubules which control urine concentration. There is a diurnal periodicity in AVP release in young, healthy
subjects, with higher AVP plasma levels in the evening contributing to decreased nighttime urine output
[58].

The diurnal variation in AVP release is absent in many older subjects. A study of 69 healthy subjects
whose plasma AVP and osmolality were monitored every four hours found that older subjects who
maintained a normal diurnal pattern in AVP had no episodes of nocturia [59]. Another study compared
diurnal AVP variation in 17 men referred for nocturia believed to be related to BPH with 10 men with no
nocturia symptoms; 11 of the 17 men with nocturia exhibited absent diurnal variation in AVP, compared
with 0 of 10 controls [60].

● Solute diuresis – Dietary solutes (principally urea, sodium, and potassium) are excreted soon after a
meal; decreased solute excretion at night is another factor accounting for relatively low nocturnal urine
output in healthy adults. Disorders in solute diuresis, associated with certain disease states, can lead to
nocturnal polyuria.

● Heart failure or other edematous states (nephrotic syndrome and venous insufficiency) causes third
spacing of fluids. Assumption of the supine position permits mobilization of some of the edema fluid into
the vascular space and leads to a solute diuresis.

● Autonomic dysfunction can increase urinary sodium excretion related to reduced sympathetic activity,
resulting in a solute diuresis [20]. Nocturnal polyuria is a frequent symptom of Parkinson disease [61].

Polyuria — Global polyuria is defined as a 24­hour urine volume that exceeds 3 liters per day (or 40 mL
per kg). Causes of polyuria (both day and night) include uncontrolled diabetes mellitus, diabetes insipidus, and
primary polydipsia. (See "Diagnosis of polyuria and diabetes insipidus".)

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Sleep disorders — Nocturia occurs in approximately 50 percent of patients with obstructive sleep apnea
(OSA) [62]. OSA should be considered as a possible diagnosis in patients with nocturia, and the close
association between the conditions has led to a suggestion that nocturia should be a screening question for
OSA [63]. Sleep disorders have been demonstrated to be a frequent cause of nocturia in men younger than
50 years [64] and in women with symptoms of daytime overactive bladder syndrome [65]. Primary sleep
disorders may result in nocturia either because of hormonal changes related to sleep­disordered breathing
[66], or due to patient misperception of the reason for awakening [67]. (See "Clinical presentation and
diagnosis of obstructive sleep apnea in adults", section on 'Clinical features'.)

Patients with a primary sleep problem (OSA, restless leg syndrome, and periodic limb movements at night)
may awaken due to the sleep disturbance but recall this as an awakening to void. In a study in a sleep clinic
population where participants were monitored with overnight polysomnography, of participants who identified
"needing to void" as the reason they awoke, the polysomnographic record showed that an apneic episode,
snoring, or restless leg movement immediately preceded the awakening in 80 percent of cases [67].

OSA may also cause nocturnal polyuria by release of atrial natriuretic peptide (ANP) due to negative
intrathoracic pressure and stretching of the myocardium [68]. ANP release causes vasodilation and inhibits
aldosterone, resulting in increased sodium and water excretion. ANP levels are elevated in patients with OSA
and nocturia [69,70] and are reduced with use of continuous positive airway pressure (CPAP) [70].

Nocturia is associated with nonrestorative sleep [71]. Individuals may be more bothered by nocturia if they
also require a longer time to return to sleep, have less total time sleeping, or report morning fatigue [46,72].

Depression — The risk of nocturia is increased in patients with untreated depression. A longitudinal study of
2000 men aged 50 to 70 years old found a relative risk of 2.8 (95% CI 1.5 to 5.2) for developing nocturia over
five years for men with depressive symptoms at study entry, compared with men with no baseline depression
[73]. Associations between symptoms of depression and nocturia have been demonstrated for adult women
(nearly twice the odds, shown in two separate studies) [10,74] and, in a single study, nearly triple the odds in
men [74]. It is not known whether treatment for depression would impact the development of nocturia.

Obesity — Abdominal adiposity is associated with a slight increased risk of having two or more episodes of
nocturia (odds ratio [OR] 1.16 comparing highest and lowest quartile) [75]. Measured abdominal girth may be
more important than body mass index.

DIAGNOSTIC EVALUATION — Patients with nocturia should have a targeted evaluation that extends beyond
the bladder (table 2) [76].

History — One question from the American Urologic Association Seven Symptom Index (AUA­7 SI) is used
frequently in clinical and research settings to identify patients with nocturia [77]: "Over the past month, how
often did you most typically get up at night to urinate from the time you went to bed at night until the time you
got up in the morning?" The validity of this question, compared with diaries and 24­hour monitoring, has been
confirmed in some [78,79], but not all [80], studies.

For most clinical purposes, the question can be shortened to:

● "On average, how many times do you wake up at night to void?"

It is also important to determine the bother or disruption caused by the nocturia:

● "Over the past month, how much has getting up at night to urinate been a problem for you?" (No
problem, very small problem, small problem, medium problem, or large problem.)

If a history of nocturia is elicited, information should be obtained regarding patterns and types of fluid intake,
medications, comorbid medical conditions, and urinary tract symptoms.

Fluid intake

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● Twenty­four hour fluid intake – Patients should be asked about the amount and types of their fluid intake.
Large fluid intakes (>40 mL/kg per day) may be responsible for nocturia. Follow­up questions about the
reason for the large fluid intake (psychogenic, history of renal stones, vigorous outdoor exercise, general
health belief about fluid intake, attempt at weight loss, diabetes insipidus) are important in developing the
treatment plan.

● Fluid intake at bedtime – Patients may drink large volumes immediately prior to bedtime. Although
clinicians should make a recommendation to reduce nighttime fluid intake, patients will often have initiated
this on their own prior to seeking help. Care should be taken not to further restrict fluid intake in older
patients who have borderline or inadequate fluid intake to meet daily needs.

● Intake of diuretic fluids – Patients should be asked about caffeine or alcohol intake prior to bedtime. Both
of these substances may predispose patients to sleep disruption at night. Caffeine usage may result in
polyuria or detrusor overactivity.

Medications — Prescription and over­the­counter medications, and their temporal relationship to nocturia
onset or worsening, should be evaluated. In particular, patients who take twice­daily loop diuretics may be
helped by switching the nighttime dose to a mid­afternoon dose [81,82].

Xanthines and beta blockers have been associated with bladder storage problems. Cholinesterase inhibitors
used for the treatment of dementia may result in worsening of lower urinary tract symptoms [83]. Conversely,
some older patients given anticholinergic medications for bladder symptoms may experience worsening
cognitive impairment or delirium [84,85].

Comorbid conditions — More than half of men and women with nocturia at least twice nightly self­
reported three or more comorbid conditions [86]. Nocturia is independently associated with hypertension,
diuretic usage, and diabetes mellitus [34], and obstructive sleep apnea (OSA) [87]. A history should also be
obtained about congestive heart failure, peripheral edema, depression, sleep problems, and nighttime pain.

The presence of dizziness may impact the ability to prescribe alpha­blocker therapy in men. Issues related to
safe ambulation at night and past history of accidental falls or injuries from falling should be explored,
particularly in older individuals.

Urinary tract symptoms — Questions should be asked about other lower urinary tract symptoms,
including obstructive symptoms (hesitancy, weak stream, incomplete emptying, or intermittency), irritative
symptoms (urinary frequency, urgency), and urinary incontinence. (See "Evaluation of women with urinary
incontinence".)

Physical examination — A comprehensive examination, similar to that performed in the evaluation of urinary
incontinence, is indicated to detect underlying health conditions and contributory factors relevant to nocturia.
The following are key points in the physical examination:

● Orthostatic vital signs are useful to measure. For older men, orthostatic hypotension and complaints of
dizziness on rising are relevant when prescribing alpha­blocker medications for benign prostatic
hyperplasia (BPH).

● The cardiovascular and pulmonary examinations should focus on evidence of volume overload or
congestive heart failure.

● The abdomen should be palpated for suprapubic masses and tenderness, although physical examination
is an insensitive test for bladder distention due to an abnormally high post­void residual.

● The rectal examination should focus on the detection of fecal impaction, resting and volitional rectal tone,
and gross estimation of prostate size (a precise determination of prostate size by digital examination is
difficult). During the rectal examination, patients can be taught how to contract their pelvic floor muscles

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while keeping their abdominal muscles relaxed. This skill can be incorporated into urge suppression
strategies.

● The lower extremities should be examined for the presence of pitting edema.

● The neurologic examination should include an evaluation of sacral root integrity by testing perineal
sensation and anal wink (visual or palpated anal contraction in response to a light scratch of the perineal
skin lateral to the anus).

Frequency­volume chart — A patient's report of average episodes of nocturia and the degree of bother is
usually adequate to assess the response to therapy. A 24­hour recording of void time and void amount, along
with times of going to bed and awakenings, can be extremely helpful in patients who have not adequately
responded to initial therapy [47], although patients may find this difficult to perform properly [78]. Such a
record can help determine whether nocturia is due to low­volume voiding at night, increased nocturnal
polyuria, or both [88]. The record provides useful diagnostic and therapeutic clues, including the maximal
voided volume (a measure of functional bladder capacity) and modal voided volume, and can identify patients
with high­volume fluid intake (≥3 liters) who did not report this in their history. A sample log is provided (form
1).

Interpretation of these records requires understanding some conventions. Nocturia episodes are voids that
occur between going to bed and rising in the morning. The first morning void is not counted as a nocturia
episode. Nighttime urine output includes any volume produced after bedtime, so this calculation does include
the first morning void. Thus, if the nocturnal urine output (amount voided during hours of sleep plus the first
morning void) is 1200 mL and the modal voided volume is 300 mL, then the patient probably has three
episodes of nocturia (1200 ÷ 300 = 4) [47]. The fourth void takes place as the first morning void and is not
counted as nocturia.

If the nighttime urine volume (1200 mL in this example, including the first morning void) divided by the 24­hour
urine volume is greater than 35 percent, the patient has nocturnal polyuria [55]. Older individuals with
nocturia, compared with older individuals without nocturia, have smaller average volume voids and a greater
percentage of their urine output is excreted at night [89].

If the voiding record shows that the 24­hour urine output is higher than expected, it is important to confirm
fluid intake. A log of the patient's complete fluid intake may be helpful.

Clinical testing — Patients with neurologic conditions affecting the bladder (including diabetic neuropathy),
older men, and those with a history of genitourinary surgery are at increased risk for urinary retention. Post­
void residual (PVR) testing by catheterization or ultrasound can be helpful in patients who might have bladder
outlet obstruction (BOO) or urinary retention. Patients found to have suprapubic distention or fullness on
physical examination should be further assessed by ultrasound or office in­and­out catheterization to
determine if there is an elevated PVR.

While parameters for interpreting the PVR results are neither standardized nor well­tested, the results might
lead one away from prescribing a bladder relaxant medication in patients with an increased PVR. In general, a
PVR of less than 50 mL is considered adequate emptying, and a PVR greater than 200 mL may require
referral for further evaluation [90].

Although measurements of urinary peak flow rate, as well as PVR, are included in all clinical trials of nocturia
involving male subjects, there is no definitive evidence stating that results from these tests are necessary in
directing choice of initial therapy. Men with low flow rates may report urinary intermittency or a long duration of
voiding. Urine peak flow can be readily measured with a flow meter. Classically, a peak flow rate greater than
or equal to 15 mL/sec (for a voided volume of at least 150 mL) makes BOO much less likely. A low flow rate
may be due to either obstruction or detrusor underactivity. In population­based studies, urine flow rates were
significantly slower among men with symptoms compared with those without symptoms; however, significant

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overlap exists [91]. Additionally, it is not clear whether men with a lower flow rate treated with BPH
medications have greater nocturia reductions than do men with higher flow rates.

Laboratory tests — Renal function, electrolytes, and serum glucose should be measured. A urinalysis
should be performed in all patients, with urine culture if an infection is suspected. In older women, the
interpretation of the urine culture must take into account the high prevalence of asymptomatic bacteriuria,
which is not a cause of either incontinence or morbidity. (See "Approach to the adult with asymptomatic
bacteriuria".)

Urine cytology and cystoscopy are indicated only if hematuria or pelvic pain is present. Patients with
undiagnosed prostate cancer are not more likely to have urinary symptoms. Nonetheless, prostate­specific
antigen (PSA) testing is reasonable in the evaluation of men with nocturia and other lower urinary symptoms
(see "Clinical manifestations and diagnostic evaluation of benign prostatic hyperplasia"). The Medical
Treatment of Prostate Symptoms study showed that patients with lower PSA values (<1.4) are less likely to
benefit from 5­alpha­reductase inhibitors than those with higher PSA values [92].

ASSESSING TREATMENT OUTCOMES — The most commonly used measure of nocturia treatment
efficacy is a reduction in nocturia episodes. Cure, or the complete resolution of nocturia, is infrequently
achieved and probably unrealistic to expect [41]. It is important to recognize that most reports of treatment
have shown only a small reduction in episodes of nocturia, ranging from 0 to 0.8 fewer episodes of nocturia
versus placebo.

An additional important target for therapy is the reduction in bother due to nocturia. Patient­based outcomes
may be assessed using general satisfaction questions or urinary incontinence­specific quality­of­life
measures.

INITIAL MEASURES — Initial treatment includes adjustment of fluid intake, especially if fluid intake is
excessive [93]. Trials of fluid modification and caffeine reduction in women with incontinence have shown
decreases in total 24­hour urinary frequency, but not specifically in nocturia [94]. A randomized trial showed
little effect on nocturia by variation in fluid intake [95]. In addition to participant difficulty in complying with the
recommended changes in fluid intake, reducing fluid by 50 percent resulted in a statistically insignificant
increase in nocturia episodes (1.4 to 1.8), and increasing fluids by 25 or 50 percent had no effect on nocturia.
Using fluid management as a part of an overall multicomponent management strategy may be useful [96,97].

Optimizing treatment for underlying conditions, such as diabetes or congestive heart failure, is important but
has not directly been shown to reduce rates of nocturia. Patients needing twice­daily diuretic medications may
be helped by moving the nighttime diuretic dose to the mid­afternoon. Treatment of peripheral edema by
compression stockings or afternoon elevation of the legs has been shown to be useful as part of a
multicomponent intervention [97].

Treatments aimed at minimizing the bother from nocturia may be helpful, even if there is no effect on the
nocturia itself. As an example, the use of a handheld urinal or a bedside commode may be helpful for patients
bothered by trips to and from the bathroom at night.

BEHAVIORAL THERAPY — Behavioral therapy, with an emphasis on pelvic floor muscle exercises (PFME,
or Kegel exercises) and urge­suppression strategies, has proven useful in women with nocturia and urge­
predominant urinary incontinence [76,98,99]. PFME strengthen the muscular components of the urethral
closure mechanism using principles of strength training: small numbers of isometric repetitions at maximal
exertion. The basic recommended regimen is three sets of 8 to 12 slow­velocity contractions sustained for six
to eight seconds each, performed three or four times a week and continued for at least 15 to 20 weeks [100].
(See "Patient education: Pelvic floor muscle exercises (Beyond the Basics)".)

In one randomized, controlled study in older women (n = 131) with urge or mixed incontinence and nocturia, a
multicomponent behavioral training program reduced nocturia by a median of 0.5 episodes per night.
Behavioral training was significantly more effective than drug treatment (median reduction = 0.30 episodes) or

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placebo (no reduction) [101]. Studies examining the benefit in men of the addition of PFME to alpha­blocker
therapy have also shown similar beneficial reductions in nocturia [102,103].

PHARMACOLOGIC THERAPY — Medications can be helpful for the treatment of nocturia associated with
bladder overactivity, bladder outlet obstruction, and nocturnal polyuria. It should be noted that exclusion
criteria for participation in some clinical trials may differ and thereby influence results by eliminating patients
less likely to respond to a specific medication.

Alpha­blocker agents (men only) — Prostatic tissue contains alpha­1 and alpha­2 adrenergic receptors.
Alpha­1 receptors are abundant in the prostate and base of the bladder, and sparse in the body of the
bladder. Alpha­1­adrenergic antagonists target the dynamic component of bladder outlet obstruction and can
reduce several benign prostatic hyperplasia (BPH) symptoms, including nocturia.

However, reductions in nocturia with alpha blockers are modest (on average net 0.2 to 0.4 fewer episodes
versus placebo) [104]. Nocturia response to alpha blockers is significantly less than the response of other
BPH­related symptoms. In one secondary data analysis, nocturia reduction of 50 percent or greater occurred
in 39 percent of men treated with terazosin, compared with 22 percent of men treated with placebo [104]. This
relatively small effect in research trials with populations selected to have the best chance for benefit and
carefully monitored for compliance [92,105] suggests that nocturia response in the general population will
likely be even more minimal.

If patients do experience a reduction in nocturia, the onset is rapid (within weeks to a month), compared with
5­alpha reductase inhibitors (see '5­alpha­reductase inhibitors (men only)' below). On the other hand, the
least expensive alpha blockers (terazosin and doxazosin) are often associated with dizziness and orthostatic
hypotension, which may be of particular concern in patients with nocturia. These side effects can be
minimized with gradual dose titration. The annual cost of tamsulosin and alfuzosin is significantly higher
(approximately fourfold), but these drugs require no dose titration, and the incidence of dizziness and
orthostasis is reduced (1 to 2 percent) [106,107]. (See "Medical treatment of benign prostatic hyperplasia".)

The presence of alpha­adrenergic receptors in the bladder outlet and neck provides a theoretic basis for the
potential effectiveness of alpha­blockers in women with nocturia [108]. Alpha­blocker therapy did not provide
relief for nocturia in women in one study [109].

5­alpha­reductase inhibitors (men only) — 5­alpha reductase inhibitors decrease nocturia by reducing the
size of the prostate gland. Treatment for four to six months is generally needed before prostate size is
sufficiently reduced to improve symptoms. The type 2 form of 5­alpha­reductase catalyzes the conversion of
testosterone to dihydrotestosterone in prostatic and other androgen­sensitive tissues. (See "Medical
treatment of benign prostatic hyperplasia".)

The efficacy of long­term therapy with 5­alpha reductase inhibitors was evaluated in the Medical Therapy of
Prostatic Symptoms (MTOPS) trial [92]. Compared with previous studies that showed no benefit of finasteride
on lower urinary tract symptoms [105] or nocturia [104], the MTOPS study demonstrated benefit with
finasteride on a combined endpoint of reduction of BPH symptoms, need for intervention for urinary retention,
and reduction of urinary symptoms. The MTOPS study also showed that combination therapy (finasteride plus
doxazosin) was superior to therapy with either single agent. However, the net benefit of combination therapy
compared with placebo, with respect to nocturia, was small, with a difference of less than 0.2 fewer nightly
episodes at one­ and four­year follow­up [110].

There are small studies suggesting that the addition of hydrochlorothiazide to alpha­blocker therapy might be
useful when treatment results from alpha­blocker therapy alone are unsatisfactory [111].

Bladder relaxant therapies — Bladder relaxant medications allow for an increase in the bladder capacity
and may reduce nocturia by both decreasing urge­associated voids and increasing bladder capacity. Agents
differ in efficacy, side effects, costs, and impact on comorbid conditions that may improve or be exacerbated
by the drug.

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Anticholinergics with antimuscarinic effects are frequently prescribed for nocturia. Several studies of these
drugs have failed to demonstrate benefit for nocturia and remain unpublished [91]. In studies that have shown
benefit, the absolute benefit over placebo in terms of nocturia reduction has been small [101,112,113]. These
agents may be most useful for nocturia in combination with a second drug [114]. (See 'Combination therapy'
below.)

While many practitioners are comfortable prescribing bladder relaxants for women, there is concern that these
agents may predispose men to urinary retention. Urodynamic studies have shown a small increase in the
post­void residual (PVR); although statistically significant, this small change has not proven to be clinically
meaningful [115,116] and these drugs have been used successfully, with clinical monitoring, in older male
patients [102,117].

Oxybutynin — Oxybutynin is the most commonly used bladder muscle relaxant. It has direct
antispasmodic effects and inhibits the action of acetylcholine on smooth muscle. Oxybutynin is available in
immediate release (IR), extended release (ER), and transdermal formulations. In one randomized controlled
study in 131 older women with urge or mixed (urge predominant) incontinence and nocturia, IR oxybutynin
(started at 2.5 mg twice daily and titrated, as needed, up to a total daily dose of 15 mg) significantly reduced
nocturia by 0.30 episodes per night, compared with control (no reduction) [101]. A similar effect size was seen
in men with the addition of titrated oxybutynin XL added to tamsulosin 0.4 mg [102].

Little is known about the comparative efficacy of oxybutynin IR versus ER for nocturia. The ER formulation
has fewer side effects (particularly less dry mouth), but the IR theoretically might be preferred for nocturia if
only nighttime usage is required. A single nighttime dose of oxybutynin IR 2.5 or 5 mg might be useful for
some patients with nocturia.

Tolterodine — In a 12­week randomized study in patients with nocturia (mean 2.5 episodes nightly, n =
850), tolterodine extended release 4 mg, compared with placebo, did not significantly reduce the total number
of nocturnal micturitions but did reduce nocturnal urgency [118]. In another study, 12­week nighttime
frequency was significantly reduced in men by approximately 0.3 episodes for those participants on
combination therapy with tamsulosin 0.4 mg and tolterodine ER 4 mg [119]. Dry mouth is the most common
side effect.

Solifenacin — Solifenacin 10 mg significantly decreased episodes of nocturia (­0.71 versus placebo ­0.52)
[112]. A pooled analysis of four randomized phase III trials found similar results for doses of 5 or 10 mg of
solifenacin, although the study considered only patients with overactive bladder who did not have nocturnal
polyuria [120]. Again, the net change in nocturia (­0.1 to ­0.2) is small [112,120], although patients do report
subjective improvement from treatment [121]. The most common side effects were dry mouth, constipation
and urinary tract infection [122].

Topical vaginal estrogen therapy (women only) — In addition to its efficacy in treating other genitourinary
symptoms of menopause (eg, vaginal atrophy), topical estrogen may decrease nocturia in women. A
systematic review of studies evaluating topical estrogen for the treatment of nocturia in postmenopausal
women reported that 60 percent of the studies demonstrated benefit [123]. There did not appear to be a
difference in efficacy or safety among the different preparations (vaginal tablets, ovules, creams, gels, or
rings). For postmenopausal women with continued nocturia despite other treatments, it is reasonable to add
topical vaginal estrogen to other therapies (table 3). (See 'Initial measures' above and 'Behavioral therapy'
above and "Treatment of urinary incontinence in women", section on 'Topical vaginal estrogen' and
"Treatment of genitourinary syndrome of menopause (vulvovaginal atrophy)", section on 'Vaginal estrogen
therapy'.)

Antidiuretic therapies

Desmopressin — Desmopressin (1­deamino­8­D­arginine vasopressin, ddAVP) is appropriately used for

younger patients (≤65 years of age) who have bothersome nocturia despite treatment above (behavioral and
other pharmacologic therapy) and who have normal baseline sodium levels. ddAVP has potentially severe
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side effects, its use should be monitored, and it should not be prescribed for most older adults (over the age
of 65). Desmopressin is used in Europe for treatment of adult nocturia under the age of 65. It is not approved
for this indication in the United States, although it is frequently prescribed off­label. ddAVP is a neuropeptide
that differs from endogenous vasopressin by a two­amino acid substitute of arginine vasopressin (AVP) which
gives the compound potent antidiuretic effect but no vasopressor activity [124].

The pathogenesis of nocturnal polyuria has been linked to either inadequate nighttime levels of AVP [125] or
inadequate diurnal variation of AVP [126]. ddAVP, taken two hours prior to bedtime, reduces nighttime urine
production (with a compensatory, and necessary, increase in daytime urine production). The initial aim of
therapy with ddAVP is to reduce nocturia and thereby provide adequate sleep; daytime diuresis should be
addressed subsequently.

Desmopressin is available as a nasal spray with dependable absorption. However, the oral tablet, with a
shorter half­life, is the most commonly used formulation for treatment of nocturia [127]. Oral ddAVP is
available in 0.1, 0.2, and 0.4 mg doses. Absorption from the gastrointestinal tract is limited (about 5 percent),
and therefore the oral form has about one­10th to one­20th the potency of the nasal form. The initial oral dose
for nocturia is 0.1 mg, though some suggest a 0.05 mg starting dose. The tablet should not be taken with
meals, in order to maximize absorption, and should be started at the lowest possible dose [128­130].

Serum sodium levels should be monitored within three days of initiation of therapy and can be titrated to a
higher dose if no hyponatremia is observed [131]. ddAVP, due to its prolonged duration of action, can result in
free­water excess and hyponatremia. Severe hyponatremia has occurred even within the context of a clinical
trial with enhanced, structured monitoring and lower­dose desmopressin [129]. Unrecognized hyponatremia
may result in seizures or be life­threatening [132]. The frequency of reported hyponatremia with ddAVP
ranges from 3 to 30 percent, with a pooled estimate of 7.6 percent (95% CI 3.7­15.1) from studies completed
as of 2003 [133]. Most trials of ddAVP exclude patients with urinary urgency, poorly controlled diabetes
mellitus, cardiac disorders, and those taking diuretics. The risk of hyponatremia with ddAVP increases 10­fold
in patients with cardiac disease [131].

Older patients are at greater risk of developing hyponatremia with ddAVP [131], likely due to a prolonged high
plasma level of ddAVP with increased age [132]. Additionally, older patients have a greater likelihood of taking
other medications (such as diuretics, nonsteroidal antiinflammatory drugs, antidepressants, or
carbamazepine) that can also depress sodium levels [134].

Although nocturnal polyuria is a more common cause of nocturia in older adults, we recommend that patients
over age 65 years not be treated with desmopressin. Older patients with baseline low normal sodium have a
75 percent incidence of hyponatremia with ddAVP therapy [135]. In addition, a pilot study of 16 male patients
(mean age 76.3 years) treated with desmopressin for one to five days found increased calcium and
decreased potassium excretion, with potential consequences of increased risk for osteoporosis, urolithiasis,
and hyperkalemia [136].

Several randomized trials have found ddAVP to be effective in treating men with nocturia [129,137­139]. A
2014 meta­analysis of 10 placebo­controlled randomized trials found that desmopressin doses of ≥0.025 mg
decreased nocturnal voids and increased time to first void [130]. A dose of 0.1 mg provided one additional
hour of sleep before the first void and 0.72 fewer voids a night. Higher doses did not provide further benefit.

An orally disintegrating tablet formulation of ddAVP, not yet available in the United States, has been studied in
men and women [140]. The minimal effective dose for men was 100 mcg (mean nocturia change ­1.38 versus
­0.84 for placebo) and 25 mcg for women (mean nocturia change ­1.22 versus ­0.88 for placebo).
Hyponatremia was more prevalent at higher doses, in older individuals, and in women [141].

OTHER TREATMENT STRATEGIES

Surgical therapy for BPH — Prostatectomy for benign prostatic hyperplasia (BPH) relieves many
symptoms, but nocturia is the symptom that persists most frequently following surgery [142]. Some have

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suggested that BPH is often mistakenly implicated as the cause of nocturia in men [143].

Posterior tibial nerve stimulation — Posterior tibial nerve stimulation (PTNS) involves transcutaneous
needle nerve stimulation near the ankle, approximating pudendal nerve stimulation. PTNS has been studied
in a sham­controlled randomized trial, evaluating the number of nocturia episodes in 214 patients with
overactive bladder [144]. The number of nocturia episodes in the group assigned to weekly PTNS for 12
weeks decreased compared with sham control (a decrease of 0.7 versus 0.3 episodes from a baseline of 2.9
nightly episodes). Improvement in nocturia was sustained over a 12­month period (0.8 episodes less than
baseline) when participants had additional treatment on an average of every two to three weeks. It is not
known if these gains would be maintained without ongoing treatment [145].

Medication for associated sleep disorders — There are few studies that have focused on treatment of
nocturia with the use of medications for sleep. One randomized study investigated melatonin as a potential
treatment for nocturia associated with bladder outlet obstruction (BOO) in older men [146]. Baseline
frequency of nocturia was 3.1 episodes per night. Melatonin (­0.32 episodes per night change) showed a
trend towards reduction in nocturia compared with placebo (­.03 and ­0.05 episodes respectively) and
significantly reduced reported bother. For adults aged 60 and older with concurrent insomnia and nocturia,
behavioral treatment directed solely at insomnia improved self­reported nocturia (­0.46 episodes) compared
with an informational control group [147].

Physical activity — While there is evidence that increased physical activity is associated with decreased
lower urinary tract symptoms, no randomized trials have shown reductions in nocturia [148].

Afternoon diuretic therapy — Several small studies have evaluated the effectiveness of an afternoon
diuretic dose on nocturia. In two randomized double­blinded studies, nocturia was reduced by approximately
0.5 episodes per night [81,82]. One trial found greatest benefit in men with enlarged prostates [81], the other
in men with nocturnal polyuria [82]. This strategy is likely to be useful in the proper population, but studies
have incompletely identified which participants are likely to benefit from this approach. Combining antidiuretic
therapy (at bedtime) with diuretic therapy (six hours prior to bedtime) increased the effect size of reduction of
nocturia but was accompanied by hyponatremia in several cases [149].

Combination therapy — As nocturia is a manifestation of various conditions (ie, overactive bladder, benign
prostatic hyperplasia, congestive heart failure, poorly controlled diabetes, peripheral edema, obstructive sleep
apnea [OSA]), numerous treatments are potentially helpful. The Third International Consultation on
Incontinence specifically recommended use of multicomponent interventions to treat lower urinary tract
symptoms in older adults [150].

Single­agent therapies available for nocturia are limited in their effectiveness, as they cannot address all of
the relevant causes of nocturia. Conditions with multiple causes can be most effectively addressed by
multicomponent interventions [151,152]. Data from a case series has shown a statistically significant mean
reduction of 1.2 episodes of nocturia per night for male patients with nocturia (n = 55) using a multicomponent
intervention individualized to the patient, which variably incorporated two of three medications (bladder
relaxant, alpha­blocker and/or sedative hypnotic), diabetes management, sleep hygiene, fluid management,
and daytime compression stockings [52]. Accompanying this change was a mean two­point improvement on a
five­point scale assessing bother impact.

SUMMARY AND RECOMMENDATIONS

● Nocturia is defined as any waking at night to void, although two or more awakenings are most often
considered clinically significant. It may be more beneficial to try to reduce the bother caused by the
nocturia than to target a specific reduction in nocturia episodes. (See 'Introduction' above.)

● Providers must be alert to reports of nocturia and inquire about nocturia if a patient has sleep difficulties.
(See 'Clinical presentation' above.)

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● Nocturia may be caused by conditions or disorders that result in low bladder volume voids, nocturnal
polyuria, or sleep disturbances. Age, benign prostatic hyperplasia, congestive heart failure, renal disease,
sleep apnea, diabetes mellitus, and diabetes insipidus are some of the conditions associated with
nocturia. Many patients have multiple etiologies. (See 'Pathophysiology' above.)

● Evaluation for nocturia should focus on patterns of fluid intake, other urinary symptoms, and a
comprehensive physical examination. Fall risk at night should be considered. A basic chemistry profile
including serum glucose should be obtained. (See 'Diagnostic evaluation' above.)

● A frequency­volume chart (ie, a voiding diary) may be helpful in determining the type of nocturia.
Nocturnal polyuria is defined as the excretion of ≥35 percent of the 24­hour urine output during the hours
of sleep. (See 'Frequency­volume chart' above.)

● Initial measures should include adjustments in timing of fluid intake and eliminating nighttime diuretic use
if present. Pelvic floor exercises and a urinal or commode near the bed may be helpful. (See 'Initial
measures' above and 'Behavioral therapy' above.)

● Single­agent therapies for nocturia have limited impact on the number of episodes. We suggest trials of
alpha­blockers with or without 5­alpha reductase inhibitors in men with nocturia related to benign prostatic
hyperplasia (BPH) (Grade 2B) and trials of bladder muscle relaxants for patients with low­volume voids
(Grade 2B). For postmenopausal women with continued nocturia despite other treatments, it is
reasonable to add topical vaginal estrogen to other therapies (table 3). (See 'Pharmacologic therapy'
above.)

● For younger patients (≤65 years of age) who have bothersome nocturia despite treatment above
(behavioral and other pharmacologic therapy) and who have normal baseline sodium levels, we suggest
treatment with ddAVP (Grade 2B). These patients must be able to recognize and report subtle changes
in fluid and weight status, and be willing to have sodium levels monitored closely. Use of ddAVP for
nocturia treatment is off­label (non­US Food and Drug Administration [FDA] approved) in the United
States. ddAVP has potentially severe side effects and should not be prescribed for most older adults
(over the age of 65). (See 'Desmopressin' above.)

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GRAPHICS

Factors potentially causative of nocturia

Mechanism Condition Diagnostic criteria

Small­volume Urgency, sometimes with urge Daytime voids ≥8, urgency, nocturia, and urge incontinence
bladder voids incontinence, urinary frequency
(>8 voids/24 hours), and/or
nocturia

Benign prostatic hyperplasia BPH: AUA­7 SI >8 and peak uroflow between 4 and 15
(BPH) or bladder outlet mL/sec; BOO: evidence of obstruction, including peak uroflow
obstruction (BOO) less than 15 mL/sec

Urinary tract infection Leukocyte esterase on U/A; presence of white blood cells >5
HPF on microscopic examination; >1000 colony­forming units
by culture

Low bladder capacity Cystometric capacity less than 150 mL

Increased Nocturnal polyuria 35 percent or more of 24­hour urine output occurring during
urine output at sleep hours, may be related to loss of diurnal variation or
night deficiency for arginine vasopressin

Peripheral edema (without heart Presence of pitting edema 10 cm above ankle

failure)

Congestive heart failure (HF) Echocardiographic evidence of a LVEF <35 percent; presence
of S3; bilateral lung crackles; use of an ACE inhibitor for HF

Poor control of diabetes Random glucose >200 mg/dL (11.1 mmol/L); glucosuria on
mellitus urine dipstick

Excessive fluid intake Analysis of self­reported intake or recorded voiding diary or

throughout day or large fluid fluid intake record
intake immediately prior to
bedtime

Intake of diuretic substances Analysis of self­reported intake

Sleep­related Difficulty with sleep Self­reported sleep latency of >30 minutes following first
disorders maintenance awakening for nocturia

Sleep apnea Daytime sleepiness, loud snoring, witnessed breathing

interruptions, or awakenings due to gasping or choking in the
presence of at least five obstructive respiratory events per
hour of sleep*

Restless leg syndrome or History, partner report, or nighttime sleep study

periodic limb movements

Unknown Hypertension >140/90 mmHg supine

mechanism

AUA SI: American Urological Association Symptom Index; U/A: urinalysis; HPF: high powered field; ACE: angiotensin­
converting enzyme; LVEF: left­ventricular ejection fraction.
* Epstein, LJ, Kristo, D, Strollo, PJ, et al. Clinical guidelines for the evaluation, management, and long­term treatment of
obstructive sleep apnea in adults. J Clin Sleep Med 2009; 5:263.

Graphic 67664 Version 3.0

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Summary of important diagnostic considerations in the evaluation of the patient

with nocturia

Element Specific aspect Rationale

History Review of medical history Heart failure, diabetes mellitus, hypertension, obstructive sleep apnea,
and peripheral edema particularly relevant; narrow angle glaucoma is a
contraindication for bladder relaxant therapy

Fluid intake Evaluation for excessive fluid intake (psychogenic polydypsia, health
belief)

Medications, especially Late afternoon or evening diuretic use may cause nocturia
for diuretics

Sleep and related Information about nighttime pain, depression, or insomnia or difficulty
conditions with sleep maintenance is important

Dizziness, low blood May be a contraindication for nonselective alpha­blocker therapy

pressure or orthostasis,
or history of accidental
falls

Dementia or mild May be contraindication, use antcholinergic drugs with caution

cognitive impairment

Physical Supine and orthostatic Particularly if alpha­blocker therapy (for men) is considered
examination blood pressure

Cardiovascular and Examination for fluid overload or heart failure

pulmonary examination

Abdominal examination Evaluation for suprapubic distention and tenderness (insensitive, but
highly specific if found)

Rectal examination Evaluation for prostate size, rectal masses, or fecal impaction; analysis of
resting and volitional contraction (useful for employing behavioral
therapy, including urge suppression strategies)

Neurologic examination Neurologic conditions (spinal cord injury or multiple sclerosis)

Laboratory Urinalysis Urinary tract pathology, hematuria

studies
Electrolyte panel Evaluation for abnormal renal function; check for glycemic control in
patients with diabetes mellitus; examination for low serum sodium
(especially for consideration of desmospressin therapy or monitoring)

Frequency Nocturnal polyuria, More accurate description of patient nocturnal urinary patterns
volume functional bladder
chart capacity, total 24­hour
urine output

Additional Noninvasive Low urine flow rate (4 to 15 mL/sec) more suggestive of BPH; very low
studies uroflowometry (in men) flow rate (<4 mL/sec) may indicate need for surgical treatment

PVR by ultrasound PVR over 200 mL may be causative of nocturia or may prevent use of a
bladder relaxant

PVR: post­void residual; BPH: benign prostatic hyperplasia.

Graphic 82467 Version 2.0

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24­hour intake and void volume record

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Vaginal estrogen preparations available in the United States for treatment of

vaginal atrophy

Preparation
Available Regimen
(US trade
strengths (FDA­approved prescribing information)
name)

Vaginal ring

Estring 7.5 mcg estradiol/day, Ring is inserted into the vagina by the patient or clinician. Ring is
released over 90 days removed and replaced with a new ring every 90 days.

Vaginal insert

Vagifem 10 mcg estradiol per Insert one tablet intravaginally daily for two weeks, followed by twice
vaginal insert weekly.

Vaginal cream

Premarin 0.625 mg conjugated 0.5 gram of cream intravaginally administered twice weekly. Cyclic
estrogens per gram of regimen also listed in approved product information, but not
cream commonly used.

Estrace 100 mcg estradiol per 0.5 grams of cream intravaginally administered daily for one or two
gram of cream weeks, then reduce to twice weekly.

US: United States; FDA: US Food and Drug Administration.

Prepared with data from: FDA prescribing information available at US National Library of Medicine NIH DailyMed website
http://dailymed.nlm.nih.gov/dailymed/index.cfm (accessed on April 3, 2015).

Graphic 58506 Version 16.0

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Contributor Disclosures
Theodore M Johnson, MD, MPH Consultant/Advisory Board: Vantia [Nocturia (QOL outcome instrument ­
in development)]; Medtronic [Overactive bladder]; Astellas [Overactive bladder]. Michael P O'Leary, MD,
MPH Nothing to disclose Howard Libman, MD Consultant/Advisory Boards: Gilead Sciences [HIV
(emtricitabine, efavirenz, elvitegravir, rilpivirine, tenofovir, cobicistat)].

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi­level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.

Conflict of interest policy

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