ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: SA-PO471

One Not So Salty Lady

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical


  • Wanigatunga, Melanie, Tulane University School of Medicine, New Orleans, Louisiana, United States
  • Taggart, Jerald Luke, Tulane University School of Medicine, New Orleans, Louisiana, United States
  • Baudy, Adrian J., Tulane University School of Medicine, New Orleans, Louisiana, United States
  • Peacock, Katherine A., Tulane University School of Medicine, New Orleans, Louisiana, United States

This is unique because it discusses a patient with many episodes of hyponatremia with different etiologies in the same hospitalization. This is important because it emphasizes the significance of physiology in evaluating hyponatremia.

1. Develop an approach to hyponatremia
2. See roles of aldo and ADH in fluid balance

Case Description

A 69-year-old woman with CLL presented with weakness, poor oral intake, and was profoundly hyponatremic to 105 mEq/L with altered mental status. WBC was 160k/uL, serum osmolality 231mOsm/kg, urine osmolality 513mOsm/Kg and urine sodium <12mEq/L. Sodium improved with infusions of normal saline but she developed decompensated heart failure and nausea. She was diuresed. Sodium recovered to normal ranges after about one month, yet after fluoxetine was resumed, sodium decreased to 126 mEq/L and was refractory to normal saline. Her studies were: serum osmolality 273 mOsm/kg, urine osmolality 365 mOsm/kg, urine sodium 38 mEq/L. Fluoxetine was stopped and mirtazapine was started for depression. Sodium improved with 1.5 L/day fluid restriction as well. She was discharged to physical rehabilitation with resolution of her mental status to baseline, and lab studies within normal ranges.


At first, there was concern our patient had pseudohyponatremia from increased WBC in her blood falsely diluting her serum sodium. In CLL, patients can have pseudohyponatremia due to hyperglobulinemia. Hospital machinery is now able to separate the serum electrolytes from other blood elements to measure them properly, ruling out psuedohyponatremia for this patient from CLL.

She had hypotonic hypovolemic hyponatremia on admission; her serum osmolality was truly low and her urine sodium showed that aldosterone was increased, trying to increase total body sodium. Urine osmolality was high, showing ADH was working to increase total body water. She improved with appropriate treatment: normal saline.

Her re-development of hyponatremia was more complex. Given her nausea and decompensated heart failure, she likely had increased ADH (Sahay & Sahay, 2014). Lab studies were not consistent with SIADH, but improved with treatment for SIADH. It is important to understand the balance of aldosterone and ADH in a patient with hyponatremia as it guides treatment.


Sahay, M., & Sahay, R. (2014). Hyponatremia: A practical approach. Indian journal of endocrinology and metabolism, 18(6), 760–771.