Polyuria resident survival guide
Overview
- Polyuria is defined as urine output more than 2 L/24 hours, or 30 ml/kg/24 hours. There are 3 pathophysiologic causes of polyuria: increased thirst (idiopathic, psychogenic polydepsia, hypothalamic disease, and medications), central diabetes insipidus (DI) (decreased secretion of arginine vasopressin (AVP)), and nephrogenic diabetes insipidus (DI) (renal resistance to AVP).[1]
- Nocturnal polyuria (NP), characterized by overproduction of urine at night (more than 20%-33% of total 24-hour urine volume depending on age). It can be caused by intake, urological, nephrological, hormonal, sleep, and cardiovascular factors. [2]
Causes
Life Threatening Causes
Common causes [3] [2]
- The most common causes of polyuria are:
- Psychogenic polydipsia
- Diabetes insipidus DI (central and nephrogenic)
- Chronic kidney disease (CKD)
- Uncontrolled diabetes mellitus (DM)
- Nocturnal Polyuria (NP) can be caused by different medical conditions including:
- Congestive heart failure (CHF)
- Diabetes mellitus (DM)
- Obstructive sleep apnea (OSA)
- Peripheral edema
- Excessive nighttime fluid intake
- Abnormalities in antidiuretic hormone arginine vasopressin (AVP) secretion can cause overproduction of urine at night
- Nocturnal Polyuria Syndrome, in the absence of any medical condition, it can be due to impaired circadian release of Arginine vasopressin(AVP).
Diagnosis
- Water deprivation test combined with desmopressin administration is the diagnostic gold standard, it differentiates between the causes of the polyuria‐polydipsia syndrome.
- The c‐terminal portion of the larger precursor peptide of Arginine Vasopressin AVP (co-peptin), has been evaluated in the setting of polyuria‐polydipsia syndrome, can be useful for the differential diagnosis. [4]
Management
Diagnostic Approach
Polyuria ❑ 24-hour urine volume >3L ❑ 24-hour urine volume >50 ml/kg | |||||||||||||||||||||||||||||||||||
Urine Osmolality >300mosmol | Urine Osmolality <300[5]mosmol | ||||||||||||||||||||||||||||||||||
Solute diuresis ❑ Glucose ❑ Mannitol ❑ Contrast media ❑ High protein intake ❑ Diuretics ❑ Medullary cystic disease ❑ Resolving ATN ❑ Resolving obstruction | |||||||||||||||||||||||||||||||||||
Water diuresis ❑ Primary polydipsia ❑ Diabetes inspidous | |||||||||||||||||||||||||||||||||||
Water restriction test OR administration of hypertonic saline 0.05 mL/kg/min for 2 h | |||||||||||||||||||||||||||||||||||
Water restriction test
❑ Overnight fluid restriction should be avoided ❑ Recommend the patient to stop drinking 2-3 hours before coming to clinic ❑ Meaure urine volume every hour ❑ Measure urine osmolality every hour ❑ Measure plasma sodium concentration every 2 hours ❑ Measure plasma osmolality every 2 hours | |||||||||||||||||||||||||||||||||||
Test endpoints in adults: ❑ Urine osmolality reaches normal value (above 600 mosmol/kg) ❑ The urine osmolality is stable for 2 or 3 successive hourly measurements despite a rising plasma osmolality ❑ Plasma osmolality >295-300 mosmol/kg ❑ Plasma sodium is 145 or higher | |||||||||||||||||||||||||||||||||||
Therapeutic Approach
Treatment
- Cranial diabetes insipidus (DI) can be managed by desmopressin orally or Intranasal (rarely used).
- Partial DI can be treated with a single nocturnal dose to prevent sleep loss due to nocturia, but complete DI requires 2-4 daily doses.
Nephrogenic diabetes insipidus:
- Withdrawal of lithium therapy usually leads to reversal of lithium-induced diabetes insipid (DI). It can persist for years after lithium withdrawal, usually indicating that the patient has developed interstitial nephritis secondary to lithium.
- Thiazide diuretics reduce urine output by up to 50%, and indomethacin has also been used. Results are frequently unsatisfactory, treatment is directed at sufficient fluid intake to replace urinary losses. [1]
- Lifestyle modifications are the first intervention for the management of nocturia and nocturnal polyuria (NP) but, as symptoms progress, pharmacotherapy may be initiated.
- Antidiuretic treatment is necessary for patients with nocturia due to nocturnal polyuria (NP) because, in many patients, it treats the underlying cause (ie, insufficient secretion of antidiuretic hormone arginine vasopressin) that leads to overproduction of urine at night and has been shown to provide statistically significant reductions in nocturnal voids.
- Desmopressin (synthetic analog of arginine vasopressin), is the only antidiuretic treatment indicated specifically for nocturia due to nocturnal polyuria (NP). [2]
Do's
Don'ts
References
- ↑ 1.0 1.1 Moore K, Thompson C, Trainer P (2003). "Disorders of water balance". Clin Med (Lond). 3 (1): 28–33. doi:10.7861/clinmedicine.3-1-28. PMC 4953350. PMID 12617410.
- ↑ 2.0 2.1 2.2 Weiss JP, Everaert K (2019). "Management of Nocturia and Nocturnal Polyuria". Urology. 133S: 24–33. doi:10.1016/j.urology.2019.09.022. PMID 31586470.
- ↑ Wieliczko M, Matuszkiewicz-Rowińska J (2013). "[Polyuria]". Wiad Lek. 66 (4): 324–8. PMID 24490488.
- ↑ Nigro N, Grossmann M, Chiang C, Inder WJ (2018). "Polyuria-polydipsia syndrome: a diagnostic challenge". Intern Med J. 48 (3): 244–253. doi:10.1111/imj.13627. PMID 28967192.
- ↑ Robertson GL: Diabetes insipidus. Endocrinol Metab Clin North Am 24:549–572, 1995.