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Kidney Week

Abstract: PO1148

Cerebral Salt Wasting in a Renal Transplant Patient

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Reddy, Prashanth, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Viswanathan, Sahityan, The University of Texas Southwestern Medical Center, Dallas, Texas, United States

Hyponatremia is a common occurrence in patients with cerebral injury and is usually thought to be secondary to SIADH. Though cerebral salt wasting is documented in literature it has been debated on if it is truly a phenomenon. Among patients with CNS disease, CSW is a much less diagnosed cause of hyponatremia and remains underdiagnosed owing to the challenge of proving its existence. Here we present a patient with a CNS injury who showed clear benefit from treatment not centered around SIADH, thus pushing us to diagnose him with CSW.

Case Description

A 63yo Male with a PMHx of DDKT presented with nausea/vomiting. A cerebellar abscess from a previous biopsy site was found and he underwent a debridement and washout. On POD#4 the patient had a drop in sodium to 131. Urine studies [urine osmolarity: 789, urine Na: 72].With continued drop in sodium and orthostatic hypotension he was started on NS 75cc/hr. The sodium continued to drop to a low of 123. At that time the NS was increased to 125cc/hr. This resulted in an upswing in serum sodium to 130. A drop in NS rate was trialed with sodium dropping back to 127. The NS was eventually ramped up to 200cc/hr with good response. During the uptitration of fluids there was no significat drop in urine osmolality noted. The patient was eventually transitioned to a dose of salt tabs close to the equivalent to the amount of fluids he was receiving[5g Q4H]. He was also started on Fludrocortisone 0.1mg daily. This resulted in our ability to drop the Salt tabs to 4g Q6H with stability in serum sodium noted. He was discharged on this regimen and was noted to have stable serum sodium on follow up a few weeks later.


CSW is difficult to diagnose due to the similarities in laboratory diagnostic markers with SIADH. One major difference is that in CSW patients are usually hypovolemic. Another aspect that differs from SIADH is the approach to treatment. In SIADH a combination of fluid restriction, lasix, and salt tabs are used. What makes our case unique is the successful use of NS to correct the patient's sodium. If this was SIADH, continuous administration of NS would have dropped the sodium level. We believe we met the burden of proof to diagnose this patient with CSW. Though there may still be debate about the existence of CSW, we believe that with the difference in treatment approach it should always be considered in the differential in patients with CNS injury.