Cerebral Salt-Wasting Syndrome Workup

  • Author: Sudha Garimella-Krovi, MBBS; Chief Editor: Stephen Kemp, MD, PhD   more...
 
Updated: Mar 29, 2012
 

Approach Considerations

Failure to distinguish cerebral salt-wasting syndrome (renal salt wasting) from SIADH as the cause of hyponatremia may lead to improper therapy (ie, fluid restriction), thereby exacerbating intravascular volume depletion and potentially jeopardizing cerebral perfusion.

The following lab studies may be indicated in patients with cerebral salt-wasting syndrome:

  • Serum sodium concentration - Patients with untreated cerebral salt-wasting syndrome are often hyponatremic
  • Serum osmolality - If measured serum osmolality exceeds twice the serum sodium concentration and azotemia is not present, suspect hyperglycemia or mannitol as the cause of hyponatremia
  • Urinary output - Urine is relatively dilute and the flow rate is often high in cerebral salt-wasting syndrome; urine is usually very concentrated and the flow rate is low in SIADH

Urinary sodium concentrations

Urinary sodium concentrations are typically elevated in SIADH and in cerebral salt-wasting syndrome (>40 mEq/L). However, urinary sodium excretion (urinary sodium concentration [mEq/L] x urinary volume [L/24 h]) is substantially higher than sodium intake in cerebral salt-wasting syndrome but generally equals sodium intake in SIADH. Therefore, net sodium balance (intake minus output) is negative in cerebral salt-wasting syndrome.

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Fractional Excretion of Uric Acid and Phosphate

Uric acid

Fractional excretion of uric acid (FEUA) is defined as the percentage of urate filtered by glomeruli that is excreted in urine. It is calculated by dividing the product of (urinary uric acid [mg/mL] x serum creatinine [mg/mL]) by the product of (serum uric acid [mg/mL] x urinary creatinine [mg/mL]) and multiplying the result by 100%. Normal values are less than 10%.

Patients with either cerebral salt-wasting syndrome or SIADH can have hypouricemia and elevated FEUA. However, after correction of hyponatremia, hypouricemia and elevated FEUA may normalize in SIADH but persist in cerebral salt-wasting syndrome (renal salt wasting).[2]

Phosphate

Fractional excretion of phosphate (FEP) should be determined when evaluating patients with hyponatremia and hypouricemia. Elevated FEP suggests cerebral salt-wasting syndrome as opposed to SIADH.[2]

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Contributor Information and Disclosures
Author

Sudha Garimella-Krovi, MBBS  Clinical Assistant Professor of Pediatrics, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences

Sudha Garimella-Krovi, MBBS is a member of the following medical societies: American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Coauthor(s)

James E Springate, MD  Associate Professor of Pediatrics, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Attending Physician, Department of Pediatrics, Division of Pediatric Nephrology, Women and Children's Hospital of Buffalo

James E Springate, MD is a member of the following medical societies: American Academy of Pediatrics, American Physiological Society, American Society of Pediatric Nephrology, International Pediatric Transplant Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Erawati V Bawle, MD, FAAP, FACMG Division of Genetic and Metabolic Disorders, Children's Hospital of Michigan; Professor (Clinician-Educator), Department of Pediatrics, Wayne State University School of Medicine

Erawati V Bawle, MD, FAAP, FACMG is a member of the following medical societies: American Academy of Pediatrics, American College of Medical Genetics, American Medical Association, and American Society of Human Genetics

Disclosure: Nothing to disclose.

Barry B Bercu, MD Professor, Departments of Pediatrics, Molecular Pharmacology and Physiology, University of South Florida College of Medicine, All Children's Hospital

Barry B Bercu, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Federation for Clinical Research, American Medical Association, American Pediatric Society, Association of Clinical Scientists, Endocrine Society, Florida Medical Association, Lawson-Wilkins Pediatric Endocrine Society, Pituitary Society, Society for Pediatric Research, Society for the Study of Reproduction, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

References

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  2. Maesaka JK, Miyawaki N, Palaia T, Fishbane S, Durham JH. Renal salt wasting without cerebral disease: diagnostic value of urate determinations in hyponatremia. Kidney Int. Apr 2007;71(8):822-6. [Medline].

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  18. Levine JP, Stelnicki E, Weiner HL, et al. Hyponatremia in the postoperative craniofacial pediatric patient population: a connection to cerebral salt wasting syndrome and management of the disorder. Plast Reconstr Surg. Nov 2001;108(6):1501-8. [Medline].

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Possible mechanisms for cerebral salt-wasting syndrome. The injured brain may release natriuretic proteins that act directly on the kidney. In addition, cerebral injury may increase sympathetic nervous system activity, elevating renal perfusion pressure and releasing dopamine.
 
 
 
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