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Abstract: SA-PO465

Parkinson Disease-Induced Cerebral Salt Wasting

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

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


  • Hansen, Zachary Austin, Tulane University, New Orleans, Louisiana, United States
  • Baudy, Adrian J., Tulane University, New Orleans, Louisiana, United States
  • Chen, Jing, Tulane University, New Orleans, Louisiana, United States

Cerebral salt wasting (CSW) primarily occurs in cerebral hemorrhage but can be caused by any neurologic disease. It is due to renal salt wasting and subsequent volume contraction, but the exact mechanism is unclear. It has many overlapping features with SIADH and distinguishing the two is important as treatment differs drastically. Here, we present a case of hyponatremia and our treatment approach.

Case Description

76-year-old man with Parkinson Disease, neurogenic bladder and suprapubic catheter presented for abdominal pain and altered mental status. He was found to be volume depleted with a serum sodium (Na) of 119 that increased to 122 with 500mL of normal saline (NS). His serum osmolality (SOsm) was 249, urine osmolality (UOsm) 421 and urine sodium (Ur Na) <12. He received 13 liters of NS over the next few days and repeat labs showed Na 127, SOsm 127, UOsm 264, Ur Na 59 and Fractional excretion of Uric Acid (FE Uric Acid) 14%. His sodium dropped when IV hydration was discontinued, raising concern for cerebral salt wasting (CSW). CT head showed no acute changes, but Parkinson’s disease remained a possible cause.

After more NS, his Na was 128, increasing suspicion for CSW. NS was stopped and Na again dropped to 124 further indicating CSW. To assess this, we measured Ur Na, and UOsm before and after giving NS. Ur Na went from 88 to 128, UOsm increased, and FE uric acid remained elevated at 22%. He was still clinically hypovolemic suggesting that he was still losing Na. After the addition of salt tablets, his Na slowly began to improve, and he was discharged.


To our knowledge, this is the first case of CSW in a patient with chronic idiopathic Parkinson’s disease. CSW is a rare disorder usually associated with vascular or traumatic cerebral injury. Its pathogenesis is unclear but may be due to naturetic peptides that result in renal salt wasting with resulting volume contraction. CSW is a challenging diagnosis and is often mistaken for SIADH early in the disease course. This can affect treatment and delay accurate diagnosis. CSW tends to have high Ur Na and severe volume depletion due to sodium wasting and high urine output. Patients will have a net negative Na balance and high FE Uric Acid. Careful assessment can help differentiate this disorder from SIADH. Patients with SIADH are euvolemic and initially have high FE Uric Acid that drops with improvement of Na.