Hypernatremia Workup

  • Author: Ivo Lukitsch, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Apr 19, 2010
 

Laboratory Studies

Diagnosis of hypernatremia is based on an elevated serum sodium concentration (Na+ >145 mEq/L). It is necessary to obtain the following lab studies:

  • Serum electrolytes (Na+, K+, Ca2+)
  • Glucose level
  • Urea
  • Creatinine
  • Urine electrolytes (Na+, K+)
  • Urine and plasma osmolality
  • 24-hour urine volume
  • Plasma AVP level (if indicated)

The first step in the diagnostic approach is to estimate the volume status (intravascular volume) of the hypernatremic patient. The associated volume contraction may be mirrored in a low urine Na+ (usually < 10 mEq/L).

In the hypovolemic patient, a hypertonic urine with a UNa+ < 10 mEq/L will point towards extrarenal fluid losses (GI, dermal), whereas an isotonic or hypotonic urine with a UNa+ >20 mEq/L indicates renal fluid loss (diuretics, osmotic diuresis, intrinsic renal disease).

In the euvolemic patient with preserved intravascular volume, hypernatremia is most likely due to pure-water losses. In the presence of hypernatremia, urine osmolality normally should be maximally concentrated (>800 mOsm/kg H2 O). Measurement of the urine osmolality will allow differentiation of the following:

  • Nonrenal causes with appropriately high urine osmolality - Isolated hypodipsia, increased insensible losses
  • Renal water loss indicated by inappropriately low urine osmolality - Diabetes insipidus (often Uosm < 300 mOsm/kg H2 O [central, nephrogenic, partial, gestational diabetes insipidus])

Caveat: Unfortunately, concentrating ability tends to fall with age; the maximum Uosm in an elderly patient may be only 500-700 mOsm/kg.

To distinguish between central and nephrogenic diabetes insipidus, first obtain a plasma AVP level and then determine the response of the urine osmolality to a dose of AVP (or preferably, the V2-receptor agonist DDAVP). Generally, an increase in urine osmolality of greater than 50% reliably indicates central diabetes insipidus, while an increase of less than 10% indicates nephrogenic diabetes insipidus; responses between 10% and 50% are indeterminate. Hyperosmolar patients with an elevated AVP level have nephrogenic diabetes insipidus; those with central diabetes insipidus will have inadequately low AVP level.

If the patient has polyuria without hypernatremia and will be evaluated for diabetes insipidus, the plasma sodium has to be above 145 mOsm/kg H 2 O prior to testing (via water deprivation test, hypertonic saline).

It is also clinically very useful to calculate the free-water clearance (cH 2 O), and it is even more important to calculate the electrolyte – free-water clearance (cH 2 Oe), to estimate the ongoing renal losses of hypotonic fluid (cH 2 O = Vurine [1-(UOsm/SOsm)]; cH 2 Oe = Vurine [1-(UNa +UK)/SNa])

An example of the use of above calculations is a follows: An 80-year-old, partially demented man with poor nutritional status is admitted to the hospital because of pneumonia. Hyperalimentation with high protein supplementation is started (containing 30 mEq/L each of Na+ and K+). Following 5 days:

  • Urine output: 4 L/day
  • BUN: 20-88 mg/dL
  • Cr: Stable at 1.4 mg/dL
  • [Na+]: From 140 mEq/L up to 156 mEq/L (despite a relatively high fluid intake)
  • Posm: 342 mOsm/kg
  • Uosm: 510 mOsm/kg
  • UNa+: 10 mEq/L
  • UK+: 42 mEq/L

The free-water clearance is calculated as follows:

cH2O = 4 x ( 1 - [510 ÷ 342] ) = -2 L/day

By this calculation, taking all osmoles into account, the patient retains 2 liters of water, improving hypernatremia; however, he is actually getting worse.

The electrolyte free-water clearance is calculated as follows:

eCH 2 O = 4 (1 - [(10 + 41) ÷ 156] ) = 2.7 L/day

The etiology of the hypernatremia is now apparent; the patient is losing approximately 2.7 L of free water per day in his urine, likely secondary to osmotic diuresis from hyperalimentation.

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Imaging Studies

  • A magnetic resonance imaging (MRI) or computed tomography (CT) scan of the brain may be helpful in cases of central diabetes insipidus eventuating from head trauma or infiltrative lesions.
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Histologic Findings

Histologic findings usually are noncontributory (although they may be helpful in central diabetes insipidus).

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Contributor Information and Disclosures
Author

Ivo Lukitsch, MD  Faculty, Department of Internal Medicine, Section of Nephrology, Tulane University School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Trung Q Pham, MD  Consulting Staff, Department of Internal Medicine, Kayenta Health Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Anil Kumar Mandal, MD  Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School of Medicine

Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Eleanor Lederer, MD  Professor of Medicine, Interim Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

References
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Figure A: Normal cell. Figure B: Cell initially responds to extracellular hypertonicity through passive osmosis of water extracellularly, resulting in cell shrinkage. Figure C: Cell actively responds to extracellular hypertonicity and cell shrinkage in order to limit water loss through transport of organic osmolytes across the cell membrane, as well as through intracellular production of these osmolytes. Figure D: Rapid correction of extracellular hypertonicity results in passive movement of water molecules into the relatively hypertonic intracellular space, causing cellular swelling, damage, and ultimately death.
Table 1. Characteristics and symptoms of hypernatremia
Characteristics of hypernatremiaSymptoms related to the characteristics of hypernatremia
Cognitive dysfunction and symptoms associated with neuronal cell shrinkageLethargy, obtundation, confusion, abnormal speech, irritability, seizures, nystagmus, myoclonic jerks
Dehydration or clinical signs of volume depletionOrthostatic blood pressure changes, tachycardia, oliguria, dry oral mucosa, abnormal skin turgor, dry axillae,
Other clinical findingsWeight loss, generalized weakness
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