Nocturia

NOCTURIA
Definitions and Terminology
 Nocturia is the complaint that the individual has to wake at night one or more times to void.
 It does not specifically relate to the hours of dark, but rather to the hours of sleep.
 Nocturia frequency includes only those voids preceded and followed by sleep. Thus the first morning
void after a night’s sleep is counted toward daytime (diurnal) frequency rather than nocturia.
 An estimate of nocturnal functional bladder capacity is given by summing the volumes of all the
nocturia episodes (nocturnal voided volume) and dividing the total by the nocturnal frequency.
 The nocturnal urine production is given by adding the first morning void to the nocturnal voided
volume. It is the nocturnal urine production that determines the diagnosis of nocturnal polyuria
(NP).
 The ICS Standardisation Committee defined NP as nocturnal urine production exceeding 20% of 24-
hour output in younger adults and 33% in older adults.
 NP can also be defined as a nocturnal diuresis of greater than or equal to 0.9 mL per minute
overnight, regarding “night” as time spent in bed.
 Alternatively, it has been defined as nocturnal urine volume exceeding 10 mL per kilogram, here
referring to night as patient-reported sleeping time.
 Nocturnal enuresis signifies voiding while remaining asleep, constituting part of the nocturnal
voided volume.
 Nocturnal enuresis does not count as nocturia because the patient fails to wake when passing
urine, but it clearly must be factored into any evaluation of LUTS and nocturnal urine production
Key Points: Voided Volume and Frequency
 Nocturia is the number of voids recorded during a night’s sleep: each void is preceded and followed
by sleep.
 Nocturnal polyuria means overnight urine production exceeds 20% to 33% of total 24-hour volume
and is age dependent.
 Polyuria in a 70-kg adult is diagnosed by a 24-hour voided volume in excess of 2.8 L (>40 mL/kg).
 If nocturnal urine production exceeds the largest voided volume (nocturia index >1), it will be
inevitable that the person has to get up at night to pass urine.
Key Terms and Definitions
 Nocturia: The number of voids recorded during a night’s sleep. Each void is preceded and followed
by sleep
 Nocturnal urine volume: Total volume of urine passed during the night including the first morning
void
 Nocturnal polyuria: Nocturnal volume >20%-33% of total 24-hr volume (age dependent)
 Polyuria: 24-hour voided volume of >2.8 L in a 70-kg adult (>40 mL/kg)
 Night: The period of time between going to bed with the intention of sleeping and waking with the
intention of arising
 Night-time frequency: The number of voids recorded from the time the individual goes to bed with
the intention of sleeping, to the time the individual wakes with the intention of rising
 First morning void: The first void after waking with the intention of rising
 Maximum voided volume: The largest single voided volume in a 24-hr period
 Nocturnal enuresis: Voiding occurring during sleep

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Prevalence
 There is a clear impact of aging on prevalence of nocturia.
 Between the ages of 30 and 39 years old, nocturia prevalence is 19.9% and in those aged between
60 and 79 it is 41.2%
 In people younger than the age of 40, nocturia is slightly more prevalent in women than men; above
the age of 60, prevalence in the two genders is similar
 In general
o Younger people are more likely to manifest decreased nocturnal bladder capacity
o Whereas nocturnal urine overproduction increasingly accounts for nocturia as people age
 Presence of NP cannot be reliably predicted from daytime LUTS
 Overall prevalence of nocturia in the BACH study was 28.4%, affecting 25.2% of men and 31.3% of
women.
 Slow-wave sleep is the restorative component of sleep, occurring mainly in the first part of the
night. Thus early sleep disturbance may result in a more substantial impact on health and ability
to carry out activities of daily living.
 Overall, presence of nocturia of two or more episodes per night has a greater impact on quality of
life, but there is considerable individual variation.

Physiology of Body Water Balance

 In maintaining water homeostasis, crucial steps include:
 Tight regulation of total body water and electrolyte loads
 Relative distribution across the intracellular, extracellular, and intravascular compartments
 Specific concentrations within each compartment
 Aquaporins:
o Short and medium-term variation of renal AQP levels are important determinants of urine
volume and composition.
o Rapid adjustment of fluid balance (“trafficking”) is due to short-term variation of AQP-2
channel density and function.
o Changes in AQP-2 and AQP-3 can occur over a period of days.
 ADH:
o Is the main endocrine regulator of AQP-2 expression.
o Modifies the structure of AQP-2  increased insertion of AQP water channels at key
locations in the nephron  increased permeability for reabsorption of water
o Retained water in SIADH leads to increased body weight, hyponatremia, and blood pressure
problems
o Where there is chronic exposure to elevated levels of ADH, the phenomenon of “escape
from antidiuresis” can occur as a result of desensitization of the renal tubules, with
downregulation of AQP-2 channel
o Therefore, chronic fluid and electrolyte imbalance can create a refractory clinical problem,
unless overall balance is corrected, and time allowed for recovery
o Other hormones can also influence AQP-2, including secretin and oxytocin
Natriuresis
 Net sodium loss in urine
 Regulated by RAAS, BNP, ANP, sympathetic nervous system, intrarenal mechanisms.
 RAAS makes major adjustments to rates of renal sodium secretion (slow adjustment)
 BNP and ANP cause net sodium excretion
 Aldosterone conserves sodium

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 Natriuresis lowers blood sodium conc. and blood volume (water follows sodium into the urine).
 Sympathetic innervation can make rapid adjustments to salt balance. This may explain why global
polyuria is common following renal transplantation, with a high prevalence of nocturnal polyuria
 Intrarenal mechanisms e.g. ATP influence on epithelial sodium channels
o Excess Natriuresis can be caused by
o Medullary cystic disease
o Bartter syndrome
o Gitelman syndrome
o Diuretic phase of acute tubular necrosis
o Primary renal diseases affecting the renal tubules
o Congenital adrenal hyperplasia
NOCTURIA PATHOPHYSIOLOGY
1. Nocturnal Polyuria
a) Behavioural (e.g., excessive evening/night-time fluid intake, polydipsia, drug-induced diuresis)
b) Global Polyuria (e.g., poorly controlled diabetes mellitus, diabetes insipidus, DIDMOAD syndrome,
panhypopituitarism)
c) Release of fluid and electrolyte sequestration (e.g., congestive heart failure, peripheral oedema,
venous stasis)
d) Obstructive sleep apnoea
e) Renal tubular dysfunction (e.g., diuretic phase of acute tubular necrosis, nephrotic syndrome)
f) Hepatic failure
g) Hypoalbuminemia
 Normally  increased secretion of ADH during sleep  circadian reduction in overnight urine
production  lower volume of concentrated urine
 Loss of circadian reduction in overnight urine production is important
 Plasma ADH levels may be pathologically undetectable during night in elderly with nocturia
 CNS lesions due to CVA can affect HP axis  loss of ADH circadian rhythmicity
2. Diminished Nocturnal Bladder Capacity and/or Global Bladder Capacity
 Storage failure
o Detrusor overactivity; idiopathic or nocturnal detrusor overactivity, neurogenic bladder
dysfunction
o Increased filling sensation; overactive bladder
 Voiding failure leading to postvoid residual; bladder outflow obstruction, reduced detrusor
contractility, dysfunctional voiding, neurogenic bladder dysfunction
 Inflammatory or painful conditions(e.g., urinary tract or genital infection, bladder pain syndrome,
bladder or ureteric calculi, malignancy)
3. Sleep Impairment
 Circadian disruption (e.g., melatonin deficiency of aging)
 Anxiety disorders
 Stimulants
 Environmental
4. Cardiac Impairment
 Result in accumulation of fluid in dependent parts of the body (“third-spacing”), which can then
return to the circulating volume when the patient is recumbent.
 Older patients can demonstrate an increased body weight during the daytime, which is greater in
patients with nocturia (mean daytime weight change 0.93 kg compared with 0.60 kg in
asymptomatic patients)

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 Ordinarily, blood pressure should reduce overnight (“dipping”). In hypertensive patients, dipping of
the blood pressure overnight becomes less apparent, signifying an increased prevalence of cardiac
disease and being associated with an increased risk of nocturia
 Underlying pathophysiology of nocturia can be related to increased mean arterial blood pressure
and blunted circadian variation in ADH
5. Global Polyuria and Increased Fluid Intake
 Polyuria = Urine output > 40 mL/kg/day (= 2.8 L/day in a 70-kg adult)
 Leads to increased voiding frequency both day and night.
 The patient’s fluid intake influences urine output.
 In many cases, patients deliberately increase their fluid intake volitionally.
 It is important to consider whether polydipsia is a cause of polyuria or vice versa(20 polydipsia)
 Best known medical examples of 20 polydipsia = poorly controlled DM and DI
 If polyuria is present in a seemingly well-controlled diabetic, breakthrough hyperglycaemia and
other causes of polyuria (e.g., Impaired renal tubular function) should be considered.
 DI can be a consequence of impaired ADH secretion (neurogenic/central DI) or impaired renal
responsiveness to ADH (nephrogenic DI).
 DI can occur in conjunction with panhypopituitarism, and it is part of DIDMOAD syndrome (DI,
diabetes mellitus, optic atrophy, and deafness)
6. Pregnancy
 Pregnancy increases LUTS including nocturia
 Nocturia in pregnancy is due to increased GFR.
 Symptoms tend to begin early in pregnancy, increasing with each trimester, with a high prevalence
of nocturia by term
7. Obstructive Sleep Apnoea
 Intermittent occlusion of airway during sleep  profound hypoxia  relieved by a gasping
respiratory pattern.
 The fluctuating hypoxia pattern impairs sleep patterns directly.
 In addition, the gasping intakes of breath substantially raise intrathoracic pressures.
 Hypoxia  Pulmonary vasoconstriction  Increased right atrial transmural pressure  Increased
ANP  Increased urine output
 Risk factors for OSA include morbid obesity, acromegaly, asthma, hypertension, adult onset DM, and
craniofacial abnormalities.
 Increasing severity of OSA has been corresponds with nocturia
 Reduction in nocturia episodes is seen by OSA treatment using CPAP.
 The link between nocturia and OSA is so close that it has been suggested that nocturia is as sensitive
as snoring as a predictive symptom of OSA (Romero et al, 2010).
 OSA should be considered in any nocturia patient, even where daytime OAB is clearly apparent
8. Impaired Renal Function
 Impaired renal tubular function  failure of reabsorption of glomerular filtrate  overall urine
output rises.
 In a long-term cohort study to evaluate risk factors for ESRD (Hsu, 2009), risk factors identified were
o Male gender
o Family history of renal disease
o Old age
o Proteinuria
o Diabetes mellitus
o African- American race

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o Higher blood pressure

o Higher body mass index, and
o Higher creatinine level
 Proteinuria and excess weight = two greatest risk factors.
 Nocturia = possible novel risk factor
 Nocturia is an independent predictor of albuminuria
 This underpins value of Nocturia as a predictor of CKD, as found by PolNef Study (Krol et al, 2009).
 Numerous influences and conditions alter renal expression of Aquaporins. For example,
hypokalemia and hypercalcemia can lead to nephrogenic DI.
9. Multiple Medical Disorders
 Nocturia in elderly men is significantly related to bladder/ prostate cancer, cerebrovascular disease,
treatment of voiding disorders, cardiovascular disease, hypertension, and moderate alcohol
consumption
 Nocturia is an important nonmotor symptom in Parkinson disease; severity of neurological
impairment is the main predictor, and nocturia ranks alongside urinary frequency as the greatest
LUTS-derived adverse influence on quality of life. Nocturia in Parkinson disease generally responds
inadequately to dopamine-targeted treatment or antimuscarinics
 In stroke patients, the most frequent bothersome LUTS is nocturia (prevalence = 53%)
 Obesity is associated with nocturia.
 Metabolic syndrome, defined as the presence of at least three of waist circumference greater than
102 cm; systolic blood pressure (BP) 130 mm Hg or greater or diastolic BP 85 or greater; high-density
lipoprotein (HDL) cholesterol less than 40 mg/dL or lipid medication use; type 2 diabetes mellitus or
increased blood sugar or diabetes medication use; or triglycerides greater than 150 mg/dL, is
associated with an increased overall risk of nocturia (odds ratio 1.69)
10. Medications
 Drugs that can increase urine output include
o Diuretics
o Selective serotonin reuptake inhibitors (SSRIs)
o Calcium channel blockers, and
o Tetracyclines
 Lithium can cause nephrogenic DI in 40%.
 Certain medications can be associated with insomnia, thereby causing additional sleep disturbance
problems. Such agents include
o Central nervous system stimulants (e.G., Dextroamphetamine and methylphenidate)
o Antihypertensives (including alpha-adrenergic antagonists, beta blockers, methyldopa)
o Respiratory medications (albuterol, theophylline)
o Decongestants (phenylephrine, pseudoephedrine)
o Hormones (corticosteroids, thyroid medications)
o Psychotropics (atypical antidepressants, monoamine oxidase inhibitors, SSRIs)
o Carbidopa
o Phenytoin
o In addition, chronic use of hypnotics can lead to tolerance and dependence. As a
consequence, rebound insomnia and anxiety can arise when the medication is stopped
(hypnoticdependent insomnia).

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11. mpaired Lower Urinary Tract Reservoir Function

 Urologic causes of low nocturnal and global bladder capacity include
o OAB
o Infravesical obstruction
o Idiopathic detrusor overactivity
o Neurogenic bladder
o Bladder inflammation (e.G., Cystitis), and
o Bladder pain syndrome (BPS).
o Bladder or ureteric calculi and neoplasms of the bladder, prostate, or urethra should also be
considered.
 Nocturia is an element in the definition of OAB. The symptom of nocturia alone does not constitute
a basis for diagnosing OAB. Indeed, lying recumbent reduces detrusor overactivity in many patients.
Nonetheless, the most prevalent combination of OAB symptoms is urgency with nocturia.
 Nocturia is commonly reported in bladder pain syndrome. The original National Institute of Diabetes
and Digestive and Kidney Diseases criteria of exclusion for diagnosing interstitial cystitis state that it
should not be diagnosed if nocturia is absent. In this context, waking is often caused by pain in the
bladder. Because the cause of waking is the pain, rather than a desire to void, use of the term
nocturia in this context is not consistent with the ICS standardized LUTS terminology, even though
the pain may be reduced by voiding.

CLINICAL ASSESSMENT
 Patients are likely to present with either nocturia or fatigue-related symptoms.
 Evaluation requires a focused history and physical examination to evaluate:
o Sleep
o Conditions that might account for excessive nocturnal urine output (cardiovascular,
endocrine, neurologic, renal impairment)
o LUTS and conditions impairing bladder capacity including OAB
o Fluid intake and medication use
 The FVC is of particular importance to document
o Volume and time of each void
o Time of retiring for sleep
o Time of rising, ideally over a 3- or 4-day period or longer if patient compliance allows
 On the basis of the FVC, the following observations should be considered:
o Diurnal or nocturnal frequency
o Global or nocturnal polyuria
o Reduced bladder capacity (overall or solely nocturnal)
o Or a mixed disorder
 Nocturia due to diminished bladder capacity is of two types:
o Global decreased bladder capacity expressed by reduced maximal voided volume or typical
voided volume
o Decreased bladder capacity apparent primarily at night-time
 Sleep duration is an independent factor for nocturia.
 When polyuria is seen on the FVC, a water-deprivation test may be used to distinguish between DI
and polydipsia.
 If the water deprivation test is abnormal, a renal concentrating capacity test can distinguish
between central and nephrogenic DI by measuring urine osmolality a few hours after a dose of
desmopressin under conditions of water restriction.

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 If renal concentrating capacity is normal, any DI will be neurogenic/endocrine, for which

desmopressin therapy is usually effective.
 Reduced concentrating capacity (urine osmolalities <550 mOsm/kg) signifies nephrogenic DI.

MANAGEMENT - Key Considerations

 Health and lifestyle issues affecting sleep quality
 Optimizing management of systemic conditions
o Optimizing management of known conditions likely to affect nocturnal urine output
o Identifying previously unrecognized conditions likely to affect nocturnal urine output
o Adjusting nature and timing of drugs used to treat otherwise unrelated systemic conditions
 Managing renal fluid and solute load
o Overall volume of oral intake
o Nature and timing of fluid and solute intake
o Endogenous fluid shifts
 Increasing bladder reservoir capacity
o Reducing storage LUTS
o Improving bladder emptying in voiding dysfunction (bladder outlet obstruction, reduced
detrusor contractility)
 Hypnotics and restoration of circadian pattern
 Pharmaceutical suppression of nocturnal renal output

1. Health and Lifestyle Issues Affecting Sleep Quality

 Attention has to be given to improving the sleep environment
 Cognitive behaviour therapy and relaxation techniques are preferred where there is comorbid
insomnia
 Educating patients on consistent bedtimes, room temperature, noise, and lighting (“sleep hygiene”)
are appropriate.
 Gentle exercise leads to the deeper sleep, thence increasing the “arousal threshold bladder
volume”—this also improves day-time urinary frequency and other health-related parameters
 Depressive symptoms increase the incidence of nocturia, so mental state needs to be considered.

2. Optimizing Management of Systemic Conditions

 The list includes cardiovascular disease, endocrine disorders, renal failure, and OSA.
 However, improvement in nocturia severity as a consequence of optimizing treatment cannot be
relied on. For example, in elderly people with hypertension, addition of a thiazide for management
of nocturia in people who are already using losartan provides no additional benefit
 Part of the optimization of treatment requires adjusting the nature and timing of certain drugs
(particularly diuretics, SSRIs, calcium channel blockers, and lithium)

3. Managing Renal Fluid and Solute Load

 Behavioural interventions to manage exogenous fluid intake include patient education, caffeine and
alcohol reduction, and restriction of night-time fluids.
 Evening fluid restriction appears to reduce nocturnal urine excretion by a comparatively small
amount. In fact, a high proportion of people with nocturia, in excess of two voids per night, have
already instigated evening fluid restrictions themselves.
 Endogenous fluid shifts, the return of free water and solutes to the circulation from sequestration
sites, also need to be considered.

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 Lower limb elevation (so that ankles are above the level of the heart), sometimes combined with
compression stockings to reduce gravity-induced third-spacing of fluid in the lower extremities, is
often advised. However, clinical evidence to support their efficacy is limited.
 A peripheral edema score has been used to evaluate nocturia in men with heart failure (Siniorakis et
al, 2008). The study proposed that edema within the prostate gland is an element underlying the
symptomatology.
o Grade 1: Ankle edema
o Grade 2: Edema of the tibial and pretibial region
o Grade 3: Ascites
o Grade 4: Extreme generalized edema (anasarca); upgrading for jugular vein distension)
 Diuretics taken in the late afternoon or early evening conceivably will decrease third-spacing of fluid
and appear to help nocturia
 Nocturia response to diuretic therapy is partly predicted by alterations in baseline ANP levels.
 Combination therapy employing a diuretic with an α blocker can achieve some benefit in a subgroup
of patients, particularly those with nocturnal polyuria.

4. Increasing Impaired Bladder Capacity

 Storage LUTS and increased filling sensation counteract reservoir function of UB
 Voiding dysfunction must also be considered because the presence of a significant PVRU will impair
reservoir function; CIC at bedtime may help nocturia in this subgroup of patients.
 For patients with OAB, antimuscarinic drugs appear to be a logical choice. Generally, evening
administration of the drug is recommended. The presence of NP reduces the clinical success.
Furthermore, reduction of nocturia frequency with these drugs is marginal relative to placebo, and
there is no significant difference compared with behavioural therapy. They are not currently
licensed for nocturia as an isolated symptom.
 In men, α-adrenergic antagonists are sometimes beneficial but NP does not generally improve with
α blocker therapy alone
 Naftopidil has been used to treat men with nocturia who have not improved with Tamsulosin;
benefits were seen in men with nocturia of three or more times per night
 Celecoxib, a cyclooxygenase- 2 inhibitor, can improve nocturnal frequency and IPSS in men with BPH
 Combination pharmaceutical therapy with α-adrenergic antagonists and 5α-reductase inhibitors can
improve symptom severity, but changes beyond 1 year are of doubtful clinical significance
 In men with OAB and nocturia, combined treatment including antimuscarinic drugs can improve
symptom severity
 Combination treatment including a nonsedating hypnotic (zolpidem) leads to a subjective reduction
in nocturia episodes in men with LUTS
 Chinese herbal medicines have been used with apparent improvement of nocturia in older men
 Nocturia scores and quality of life can improve as a result of surgical treatment in men
 Following TURP, nocturia improvement is more clearly apparent in men of a lower age and with a
lower preoperative maximum flow rate
 TURP can improve nocturia frequency and quality of life, hours of undisturbed sleep, and the longest
sleep interval between voids
 However, in nocturia-predominant LUTS, the physician should fully investigate the pathophysiology
underlying the nocturia, evaluate whether bladder outlet obstruction is actually present, and warn
patients that improvement of nocturia with surgical intervention is not reliable and of uncertain
longevity

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5. Hypnotics and Restoration of Circadian Pattern

 Hypnotics can affect nocturia
 Benzodiazepine oxazepam reduced nocturia 63%, but with no effect on urine volume
 Benefits may be in improving return to sleep, rather than in improving frequency
 Those patients taking >30 minutes to return to sleep after awakening can be prescribed a non-
benzodiazepine sedative to take once per night after a first nocturia episode between 23.00 and
03.00 hours
 Can be associated with hangover sedation when rising the following morning.
 The pineal gland hormone melatonin is secreted during nocturnal hours and is a major determinant
of physiologic circadian rhythm. This release is affected in some older patients with sleep
impairment; exogenously administered melatonin can counteract some of the associated sleep
impairment and is not associated with hangover sedation.
 Melatonin in isolation has been used for treatment of nocturia in men with BPH, showing marginal
changes in the overall study group but with more overt benefits in a small subgroup of patients in
whom nocturnal frequency fell by more than one void per night
 Effect of melatonin supplementation has been compared with the hypnotic agent Rilmazafone in
elderly patients; both groups showed reduction in the number of nocturnal voids
6. Pharmaceutical Suppression of Nocturnal Renal Output
 Desmopressin can achieve significant improvement in nocturia symptoms for the isolated symptom
and when nocturia is a component of OAB.
 Desmopressin is increasingly used for management of nocturnal polyuria
 33% of men and 46% of women showed at least a 50% reduction in the mean number of voids per
night relative to baseline
 A greater proportion of patients showed at least a 50% reduction in the number of nocturnal voids
in longer-term use
 Dilutional hyponatremia with Desmopressin
o Occurs in 7.6% of patients
o Risk factors include age older than 65 years and low serum sodium at baseline
o The serum sodium concentration should be checked within a few days of instigating
treatment, and dose titration should be employed
o In long-term use, sodium should be assessed at least every 6 months
 Desmopressin is licensed for management of nocturia in multiple sclerosis (MS); its influence on
renal urine output is exerted in the 6-hour period following administration. Its value is more likely to
be clinically beneficial if maximal bladder capacity is adequate.
 Cannabis extracts also appear to help nocturia in MS
 Nonsteroidal anti-inflammatory drugs including oral Loxoprofen and Indomethacin suppositories
have been administered at bed-time for the treatment of nocturia. The mechanism of action
appears to be a reduction in nocturnal urine volume. It is not clear whether this approach risks any
long-term effects on renal function.

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Key Points: Assessment and Treatment

 The FVC is used to document key parameters determining diurnal or nocturnal frequency, global or
nocturnal polyuria, reduced bladder capacity (overall or nocturnal), or a mixed disorder.
 Symptom assessment tools are used to capture subjective elements of nocturia.
 Individualized treatment plans based on evaluation of risk factors should integrate advice and
specific instructions with directed interventions.
 Improved sleep environment, self-help, depression management, cognitive behavior therapy,
relaxation techniques, and gentle exercise are used to manage comorbid insomnia.
 Major nonurologic diseases that can contribute to nocturia are prioritized in management.
 Volume, nature, and timing of fluid and solute intake can be adjusted, while endogenous fluid shifts
also need to be considered.
 Storage and voiding dysfunction have to be managed to restore bladder reservoir function;
intermittent selfcatheterization, antimuscarinic drugs, and combination treatments can be
considered.
 For nocturia-predominant LUTS in men, comprehensive evaluation is necessary before considering
surgery to reduce the risk of a poor symptomatic outcome.
 The benefits of sedative agents may be in improving return to sleep, rather than nocturia frequency.
Treatment with melatonin can counteract sleep impairment and reduces nocturia in some patients.
 Desmopressin can achieve significant improvement in nocturia symptoms for the isolated symptom,
as well as when nocturia is a component of OAB. Dilutional hyponatremia occurs in 7.6% of patients.

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