Hypernatremia laboratory tests

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Assistant Editor(s)-In-Chief: Jack Khouri

Overview

The diagnostic work-up of hypernatremia includes many lab studies including urine osmolarity which tells whether the kidney's function is altered or not. The water deprivation test aims at diagnosing the cause of diabetes insipidus (DI). In response to water deprivation, fluid homeostatic mechanisms work to retain water by stimulating the secretion of a hormone called vasopressin (antifiuretic hormone (ADH)) from the posterior pituitary gland. Vasopressin exerts its effects on the medullary collecting ducts of the kidney where it increases water retention and thus maintaing normal osmolar balance. In patients with DI, this mechanism is impaired, either due to decreased ADH secretion (central DI) or renal resistance to ADH urine concentrating effects (nephrogenic DI) (see below for a more detailed discussion of this test). Other lab studies can be done to investigate about adrenal or thyroid disease. Brain imagery can identify any cerebral process causing hypothalamic dysfunction.

Labs and Procedures

• Urine osmolarity is essential to differentiate renal from extrarenal water loss. A normal kidney would respond to hypernatremia by excreting a highly concentrated urinewith a urine osmolality >800 mosmol/kg.
  • Urine osmolarity <300 mosm/kg is consistent with renal water losses due to diabetes insipidus (neurogenic vs nephrogenic).
  • Urine osmolarity between 300 and 800 mosm/kg indicates partial diabetes insipidus or osmotic diuresis.
  • Urine osmolarity >800 mosm/kg points out to insensible or GI losses, increased sodium ingestion or primary hypodypsia.

• The water deprivation test
  • The objective of this test is to distinguish the origin of diabetes insipidus (DI).
  • Desmopressin (AVP), a synthetic analogue of vasopressin, is an important component of this test.
  • Upon AVP adminstration, patients will have different urine osmolarities depending on their DI etiology.
  • Patients with neurogenic DI have intact kidney response to vasopressin and will have a substantial increase in urine osmolarity (>50%) in response to water deprivation and desmopressin administrarion.
  • Patients with nephrogenic DI have little or no increase in urine osmolarity in response to AVP.
  • Patients with partial central DI show a 10-50% increase in urine osmolarity.

References

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