Urinary Frequency and Polyuria
Matthew Sampson
INTRODUCTION
A perceived increase in urination is a common concern that a pediatrician may be asked to evaluate. A key task is to differentiate true polyuria from urinary frequency. Polyuria, defined formally as urine output 2,000 mL/1.73 m2 over 24 hours, is usually caused by excessive fluid intake, a lack of release of antidiuretic hormone (ADH), tubular insensitivity to ADH, or an osmotic diuresis. In rare cases, it results from relief of urinary obstruction (“postobstructive dieresis”) or is the polyuric phase of recovery from acute tubular necrosis. Urinary frequency not associated with polyuria is a common finding in children most typically caused by urinary tract infection (UTI), pollakiuria (frequent daytime urination), or chemical irritation.
DIFFERENTIAL DIAGNOSIS LISTInfectious Causes
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Pyelonephritis
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Meningoencephalitis
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Congenital cytomegalovirus and toxoplasmosis
Toxic Causes
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Recovery phase of acute tubular necrosis (typically caused by medications/toxins or hypoperfusion)
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Furosemide
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Aminoglycosides
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Phenytoin
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Demeclocycline
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Amphotericin B
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Vinblastine
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Cisplatin
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Lithium
Metabolic or Genetic Causes
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Inherited nephrogenic diabetes insipidus (NDI)
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Sickle cell disease
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Fanconi syndrome (e.g., cystinosis)
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Polycystic kidney disease
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Familial juvenile nephronophthisis
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Bartter syndrome
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Diabetes insipidus, diabetes mellitus, optic atrophy, and deafness syndrome
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Laurence-Moon-Biedl syndrome
Psychosocial Causes
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Primary polydipsia
Miscellaneous Causes
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Postobstructive diuresis
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Diabetes mellitus
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Idiopathic central diabetes insipidus
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Hand-Schüller-Christian disease
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Sarcoidosis
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Sjögren syndrome
Neoplastic Causes
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Craniopharyngioma
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Meningioma
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Glioma
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Metastasis—lymphoma, leukemia
Traumatic Causes
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Severe head trauma
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Hypophysectomy
Congenital or Vascular Causes
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Obstructive uropathy
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Cerebral hemorrhage
Urinary Frequency
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Cystitis
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Urethritis
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Constipation
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Pollakiuria
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Hypercalciuria
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Neuropathic bladder
DIFFERENTIAL DIAGNOSIS DISCUSSION
Central Diabetes Insipidus
Etiology
Central diabetes insipidus is urinary loss of water caused by impairment of vasopressin (ADH) production in the central nervous system (CNS) and may be idiopathic, acquired, or inherited. Approximately one-third of affected infants and children have the idiopathic (primary) form. Secondary causes include trauma, tumors (especially craniopharyngioma), hemorrhage, CNS infection, hypoxia, and Langerhans cell histiocytosis. The autosomal dominant form of central diabetes insipidus is rare.
Clinical Features
Children present with a sudden onset of polyuria, nocturia, and polydipsia with a predilection for cold water. Hypernatremia and dehydration do not occur if the thirst mechanism is intact and there is ample access to water. There are no specific abnormal physical findings in primary central diabetes insipidus.
Evaluation
Laboratory studies reveal a consistently low urine osmolality, but in the absence of dehydration, it is difficult to distinguish central diabetes insipidus from NDI and psychogenic polydipsia. A water-deprivation study is diagnostic for central diabetes insipidus when the serum osmolality is increased and the urine osmolality and the plasma vasopressin concentration remain decreased in the face of strict withholding of water. A brisk response, as measured by an increase in urine osmolality, to the administration of exogenous ADH is expected.
Radiographic imaging of the head is necessary to exclude secondary causes.
Treatment
Treatment consists of replacement therapy with desmopressin acetate, a synthetic analogue of vasopressin administered either intranasally or orally. The dose is adjusted to the patient’s needs. Hyponatremia can develop if the patient drinks inappropriately while on therapy. Specific treatment is recommended for secondary causes.
Inherited Nephrogenic Diabetes Insipidus
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