1318 - Altered Mental Status: A Case of SIADH and Hypertension-Induced PRES Mimicking Tacrolimus Neurotoxicity in Orthotopic Liver Transplant

Thursday, February 19, 2026

5:00 PM - 6:30 PM AST

Presenting Author(s)

NP

Nikit Patel, DO

Resident Physician
Jefferson Moss-Magee Rehabilitation
Philadelphia, Pennsylvania, United States

Co-Author(s)

SG

Surya Gourneni, MD

Resident Physician
Moss Rehab
Elkins Park, Pennsylvania, United States

Submitter(s)

NP

Nikit Patel, DO

Jefferson Moss-Magee Rehabilitation
Philadelphia, Pennsylvania, United States

Case Diagnosis: 49-year-old female following orthotopic liver transplant (OLT) with altered mental status (AMS) presumed secondary to tacrolimus neurotoxicity; however, found to have syndrome of inappropriate antidiuretic hormone secretion (SIADH) and hypertension-induced posterior reversible encephalopathy syndrome (PRES).

Case Description: This patient with alcoholic hepatitis was admitted to inpatient rehabilitation (IPR) after prolonged hospital course following OLT, complicated by renal failure requiring hemodialysis, sepsis, vocal cord paralysis requiring Dobhoff tube, and newly diagnosed breast cancer. Blood pressure was elevated on admission and remained challenging to control. Tacrolimus was monitored with transplant team input; subtherapeutic (4.3ng/ml) on admission, prompting dose increase. On day 4, she developed asymptomatic hyponatremia (130mEq/L), worsening to 124mEq/L on day 7, with tacrolimus supratherapeutic at 16.3ng/ml. Free water flushes were discontinued, and tacrolimus dose decreased. On day 8, sodium up-trended to 126mEq/L. On day 10, she developed acute AMS and was re-admitted to acute care. Labs reported worsening hyponatremia of 121mEq/L. Urine studies suggested SIADH. MRI-brain reported evidence of PRES. Nephrology and neurology were consulted; hypertonic saline was initiated. Her mental status improved with sodium correction and blood pressure management prior to discharge.

Discussions: Within IPR, tacrolimus, an immunosuppressant for solid organ transplants, requires dose adjustments based on trough levels as patients recover from prolonged hospitalization. Given our patient’s supratherapeutic trough, tacrolimus-induced neurotoxicity was a differential for her AMS. However, work-up revealed severe hyponatremia and PRES, thus, proposing alternative etiologies. Prior cases of various solid-organ transplants propose a mechanism that tacrolimus causes hyponatremia through induced aldosterone resistance1-6. Rarely, PRES can be mediated through cytotoxic effects of tacrolimus7. While it’s possible our patient developed hyponatremia and PRES due to supratherapeutic tacrolimus, further investigations revealed hypertension and SIADH as likely culprits.

Conclusions: This case highlights the importance of monitoring tacrolimus, sodium, and blood pressure in OLT patients in IPR to reduce incidence of AMS and PRES.