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Abstract: PO1146

A Rare Cause of Hyponatremia: Renal Salt Wasting Syndrome of Unclear Etiology Post Autologous Hematopoietic Stem Cell Transplant

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

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

Authors

  • Polani, Adnann Salim, Baylor College of Medicine, Houston, Texas, United States
  • Reddy, Vikas D., The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
  • Mukku, Venkata Kishore R., The University of Texas Medical Branch at Galveston School of Medicine, Galveston, Texas, United States
  • Parvathareddy, Vishnupriyadevi, Baylor College of Medicine, Houston, Texas, United States
  • Chen, Sheldon, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
Introduction

Hyponatremia is common in cancer patients. We report a rare case of acute hyponatremia in a patient with multiple myeloma (MM) who developed renal salt wasting syndrome (RSWS) as a complication of autologus hematopoietic stem cell transplant (SCT)

Case Description

A 57-year-old female with history of Plasmacytoma treated with radiation therapy that subsequently relapsed as MM with POEMS syndrome and was treated with VRd regimen presented for autologous SCT. MM was in remission and patient underwent Melphalan pre-conditioning with last melphalan dose 48 hours prior to transplant. 36 hours post-transplant patient had a seizure. Labs revealed acute drop in serum sodium from 137 to 117 over 17 hours. CT head revealed mild generalized cerebral edema. Patient also had acute polyuria (> 4 L/day). Patient was treated emergently with hypertonic saline bolus and had resolution of neurological symptoms however, serum sodium continued to drop and she required around 2 L of hypertonic saline infusion over the next 24 hours to correct sodium at desired rate. Urine studies at the time of hyponatremia revealed urine osmolality of 477, sodium 161 and potassium 34. Initial working diagnosis was SIADH that was quickly revised to RSWS based on high urine sodium, hypovolemia and polyuria. The patient was able to be transitioned to salt tablets once polyuria resolved over the next 36 hours. Urine sodium remained elevated. A repeat CT head showed resolution of cerebral edema.

Discussion

RSWS post SCT is rarely reported. Among the few reported cases an underlying CNS complication or a post-transplant hyponatremia inducing medication exposure that predated acute hyponatremia was present. Moreover the reported cases appeared to be non autologous transplants.

SIADH and RSWS (including CSWS) are similar in the sense that both present with similar urine studies. Volume status and urine output are the key factors to help differentiate between the two entities. Clinically differentiating between these two entities is important as fluid restriction is the key management in the one and solute plus volume replacement in the other. Based on our case we recommend that hyponatremia post SCT should be carefully evaluated and RSWS be considered in the differential even if there is no obvious underlying cause.