In a healthy adult without heart failure, renal disease, or diabetes (A1c 5.2%) and with normal sodium, serum and urine osmolality and copeptin, can prolonged supine positioning cause urinary frequency of about 1 L in an eight‑hour period?

Prolonged Supine Positioning and Urinary Frequency

In your specific case—with normal metabolic parameters, no heart failure, no edema, and no nocturia—prolonged recumbency alone is unlikely to be the primary cause of your daytime urinary frequency of 1047 mL over 8 hours.

Why Recumbency-Related Polyuria Is Not Your Issue

Your clinical picture argues strongly against recumbency-induced fluid redistribution as the mechanism:

• Recumbency causes nocturnal polyuria primarily in patients with heart failure, peripheral edema, or chronic kidney disease 1, 2. When lying down, gravity-dependent fluid in the lower extremities shifts centrally, increasing renal perfusion and urine output 2. However, this mechanism becomes clinically significant only when underlying cardiovascular or renal pathology is present 2.

• You have explicitly ruled out the conditions that amplify recumbent fluid redistribution: no heart failure, no edema, no kidney disease, normal blood pressure, and normal potassium 1, 2.

• Most tellingly, you do not wake at night to urinate 2. If recumbency were driving your frequency through fluid redistribution, you would experience nocturnal polyuria—defined as >33% of your 24-hour urine output occurring during sleep 3, 2. Instead, your frequency is confined to waking hours despite lying down continuously.

Your Laboratory Results Rule Out Key Metabolic Causes

Your informal water-fasting test results are reassuring:

• Copeptin 4.6 pmol/L is low-normal, effectively excluding diabetes insipidus 1. The European Association of Urology guidelines state that morning urine osmolality >600 mOsm/L after overnight fluid avoidance rules out diabetes insipidus 1. Your urine osmolality of 498 mOsm/L is borderline but, combined with low copeptin and normal sodium (143 mmol/L), makes central or nephrogenic diabetes insipidus extremely unlikely 4.

• A1c of 5.2% excludes diabetes mellitus as a cause of osmotic diuresis 2.

• Normal serum osmolality (301 mOsm/kg) and sodium (143 mmol/L) confirm appropriate water balance 1.

What You Should Actually Investigate

The most likely explanations for your daytime frequency are behavioral, bladder-based, or related to your immobility itself—not fluid redistribution:

1. Overactive Bladder (OAB)

• OAB is the most common urodynamic finding causing frequency, present in 48% of cases with urgency and frequent small-volume voids 3. The hallmark is urgency—a sudden, compelling urge to void that is difficult to defer 3.
• You need a 3-day frequency-volume chart to document voiding times, individual voided volumes, and whether urgency precedes each void 3, 5. This is the single most important diagnostic tool 3.
• If your voids are small-volume (<150–200 mL) with urgency, OAB is likely 3, 2.

2. Behavioral Factors Related to Immobility

• Xerostomia (dry mouth) from prolonged immobility, mouth breathing, or medications can drive excessive fluid intake, which then causes frequency 1, 2. The European Association of Urology specifically highlights this mechanism 2.
• Excessive fluid intake, particularly if you're drinking out of boredom or habit while lying in bed all day, will directly increase urine output 2.
• Caffeine and alcohol are bladder irritants that increase frequency 2.

3. Constipation

• Fecal retention mechanically compresses the bladder, lowering functional capacity and triggering more frequent voiding 5. This is especially relevant if prolonged immobility has caused constipation.
• Constipation must be treated concurrently with urinary symptoms because bowel dysfunction directly worsens bladder outcomes 5.

4. Sleep Disorders Masquerading as Urinary Issues

• The European Association of Urology recommends screening for obstructive sleep apnea, insomnia, and restless legs syndrome in patients with urinary frequency 1, 2. Ask yourself:
  • "Do I have problems sleeping aside from needing to urinate?" 2
  • "Do I wake up without feeling refreshed?" 2
  • "Do I fall asleep during the day despite spending all day in bed?" 2
• Sleep fragmentation from these disorders can increase perceived frequency even without true polyuria 1.

5. Medications

• Diuretics, calcium channel blockers, lithium, and NSAIDs all increase urinary frequency 3, 2, 5. Review every medication you take.

Your Next Steps

Complete a 72-hour voiding diary documenting:

• Time of each void 3, 5
• Volume of each void 3, 5
• Fluid intake timing and volume 3
• Whether urgency preceded each void 3

Calculate your 24-hour urine output and nocturnal proportion:

• If >33% occurs during sleep, you have nocturnal polyuria despite not waking to void 3, 2
• If voids are small-volume (<200 mL) with urgency, suspect OAB 3
• If voids are normal-to-large volume (>200 mL) without urgency, suspect behavioral causes (excessive intake, xerostomia) 3, 2

Address constipation if present:

• Aim for a soft, comfortable bowel movement daily, ideally after breakfast 5
• Polyethylene glycol (PEG) is the evidence-based first-line stool softener 5

Review medications and fluid intake:

• Reduce evening fluids, caffeine, and alcohol 2
• Adjust timing of any diuretics or other culprit medications 1

Critical Pitfall to Avoid

Do not assume your immobility is causing frequency through recumbency-induced fluid shifts 2. That mechanism requires heart failure, edema, or kidney disease—none of which you have 1, 2. Your lack of nocturia is the clinical clue that recumbency is not the driver 2. Instead, focus on bladder dysfunction (OAB), behavioral factors (fluid intake, xerostomia), constipation, and sleep disorders as the true culprits 3, 2, 5.