Hypernatremia laboratory tests: Difference between revisions
Jump to navigation
Jump to search
Jack Khouri (talk | contribs) |
No edit summary |
||
| (2 intermediate revisions by 2 users not shown) | |||
| Line 1: | Line 1: | ||
{{ | __NOTOC__ | ||
{{Hypernatremia}} | |||
{{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]] | {{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]] | ||
==Overview== | ==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 ( | 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]] (antidiuretic 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 maintaining 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. | ||
== | ==Laboratory Findings== | ||
* Urine osmolarity is essential to differentiate renal from extrarenal water loss. A normal kidney would respond to hypernatremia by excreting a highly concentrated | * Urine osmolarity is essential to differentiate renal from extrarenal water loss. A normal kidney would respond to hypernatremia by excreting a highly concentrated urine with 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 <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 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. | ** Urine osmolarity >800 mosm/kg points out to insensible or GI losses, increased sodium ingestion or [[primary hypodypsia]]. | ||
* The water deprivation test | * The [[water deprivation test]] | ||
** The objective of this test is to distinguish the origin of diabetes insipidus (DI). | ** 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. | ** [[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. | ** 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 | ** 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 administration. | ||
** Patients with nephrogenic DI have little or no increase in urine osmolarity in response to AVP. | ** Patients with nephrogenic DI have little or no increase in urine osmolarity in response to AVP. | ||
** Patients with partial | ** Patients with partial neurogenic DI show a 10-50% increase in urine osmolarity. | ||
==References== | ==References== | ||
| Line 30: | Line 31: | ||
[[Category:Blood tests]] | [[Category:Blood tests]] | ||
[[Category:Intensive care medicine]] | [[Category:Intensive care medicine]] | ||
[[Category:Inborn errors of metabolism]] | [[Category:Inborn errors of metabolism]] | ||
{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
Latest revision as of 19:44, 27 September 2012
|
Hypernatremia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Hypernatremia laboratory tests On the Web |
|
American Roentgen Ray Society Images of Hypernatremia laboratory tests |
|
Risk calculators and risk factors for Hypernatremia laboratory tests |
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 (antidiuretic 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 maintaining 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.
Laboratory Findings
- Urine osmolarity is essential to differentiate renal from extrarenal water loss. A normal kidney would respond to hypernatremia by excreting a highly concentrated urine with 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 administration.
- Patients with nephrogenic DI have little or no increase in urine osmolarity in response to AVP.
- Patients with partial neurogenic DI show a 10-50% increase in urine osmolarity.