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).

• 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.

Causes

Common causes

• The most common causes of polyuria are:
  • Pregnancy
  • Psychogenic polydipsia
  • Central diabetes insipidus (CDI)
  • Nephrogenic diabetes insipidus (NDI)
  • Diabetes mellitus (DM)
  • Chronic kidney disease (CKD)
  • Urinary tract infection (UTI)
  • Interstitial cystitis
  • Nephrolithiasis
  • Primary hyperparathyroidism
  • Familial hypocalciuric hypercalcemia
  • Hypercalcemia
  • Hypokalemia
  • Sickle cell disease (SCD)
  • Stroke or neurological diseases
  • Benign prostatic hyperplasia (BPH)
  • Stress incontinence
  • Medicine (Lithium,diuretics)
  • Overactive bladder
  • Drinking alcohol or caffeine

• 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.

Approach to Polyuria

Suspected hypotonic polyuria

Confirm presence of polyuria: (>50ml/kg/24hrs or >3-4L/day)

(Polyuria confirmed): Measure urine osmolality

(No polyuria/ or >800 mOsm/kg): Diabetes insipidus(DI)/Primary polydipsia ruled out

(<800 mOsm/kg): Hypotonic polyuria confirmed: Measure serum Sodium and plasma osmolality

Low normal or low serum Sodium (<150 mmol/L), plasma osmolality (<280 mOsm/kg): Primary polydipsia

Normal serum Sodium/plasma osmolality: Indeterminate diagnosis

High serum Sodium (>146 mmol/L), plasma osmolality (>300 mOsm/kg): Central or Nephrogenic DI

Water deprivation test

Baseline plasma copeptin

Hypertonic saline infusion test

Urine Osm >800 mOsm/kg

Urine Osm <300 mOsm/kg

Urine Osm 300-800 mOsm/kg

Plasma coprptin >4.9pmol/L

Plasma coprptin <4.9pmol/L

Mild primary polyuria

Desmopressin administration

>21pmol/L

<2.6pmol/L

>2.6pmol/L

(Urine Osmolality: 300-800 mOsm/Kg and <50% increase): Therapeutic trial with desmopressin

Nephrogenic DI(partial or complete)

Complete Central DI

Primary polydipsia

Partial Nephrogenic DI

Partial Central DI

(Initial urine osmolality: 30 mOsm/kg and >50% increase after desmopressin): Complete Central DI

(Urine osmolality <300 mOsm/kg or <50% increase): Complete Nephrogenic DI