Kidney Week

Abstract: FR-PO0994

Magnesium Sulfate Truncation in Severe Preeclampsia with Hemolysis, Elevated Liver Enzymes, Low Platelet Count (HELLP)-Associated AKI: Balancing Toxicity Risk and Seizure Prophylaxis

Session Information

• Women's Health and Kidney Diseases
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Women's Health and Kidney Diseases

• 2100 Women's Health and Kidney Diseases

Authors

• Khalifa, Muhammed, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States

Muhammed Khalifa, MD

• Ibrahim, Abdelrahman, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States

Abdelrahman Ibrahim, MD, MBChB

• Gad, Ahmed, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States

Ahmed Gad, MD, MBChB

• Mekki, Ossama, University of Utah Health, Salt Lake City, Utah, United States

Ossama Mekki, MD, MBChB

• Puscar, Candela, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States

Candela Puscar, MD

• Kwakye, Kwabena A., Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States

Kwabena A. Kwakye, MD

Group or Team Name

• HCMC Chief’s Office

Introduction

Magnesium sulfate is standard therapy for seizure prophylaxis in preeclampsia with severe features and is typically continued for 24 hours postpartum. Because magnesium is renally cleared, acute kidney injury (AKI) increases risk of accumulation and toxicity, yet no clear guidance exists for magnesium use in severe obstetric AKI.

Case Description

A 17-year-old G2P1 presented with preeclampsia with severe features and underwent spontaneous vaginal delivery on the day of admission. Postpartum course was complicated by HELLP syndrome with severe AKI, thrombocytopenia, and hemolysis. Creatinine rose from 1.50 to 5.34 mg/dL within 96 hours, prompting nephrology consultation. Magnesium sulfate was initiated postpartum per standard protocol. However, worsening renal function raised concern for impaired magnesium clearance and toxicity risk. Although she remained non-oliguric and did not meet indications for kidney replacement therapy, magnesium was discontinued after 17 hours, when creatinine had risen to approximately 4.4 mg/dL, rather than the standard 24. Serum magnesium levels were not serially trended, but neurologic status, respiratory effort, and urine output were closely monitored. She developed no clinical evidence of magnesium toxicity or eclamptic seizure. Hemodialysis was not required. Renal function recovered gradually, with creatinine improving to 4.02 mg/dL by discharge on postpartum day 6.

Discussion

This case highlights a nephrology-specific dilemma in severe obstetric AKI: balancing seizure prophylaxis against reduced renal magnesium clearance. Standard postpartum magnesium protocols assume preserved kidney function and may not be appropriate in severe AKI. Here, marked creatinine elevation without dialysis indication created a therapeutic gray zone in which nephrology input guided deviation from routine magnesium exposure despite persistent seizure risk. The absence of toxicity or seizure after early discontinuation suggests magnesium duration may require individualized adjustment in HELLP-associated AKI. Nephrology-informed magnesium protocols in pregnancy-associated AKI should incorporate renal function, urine output, and bedside toxicity monitoring.