Abstract: TH-PO0410
Hyperkalemic? Don't Miss the Mag!
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Alam, Mariam, Mercy Health St. Rita's Medical Center, Lima, Ohio, United States
- Hartsell, Sydney Elizabeth, University of Utah Health, Salt Lake City, Utah, United States
- Abraham, Josephine, University of Utah Health, Salt Lake City, Utah, United States
Introduction
Magnesium is widely used in peripartum care, with a risk of iatrogenic magnesium toxicity. Hyperkalemia is an often-overlooked consequence of hypermagnesemia.
Case Description
A 36-year-old woman at 36w6d gestation was admitted in labor complicated by placenta accreta, requiring emergent c-section and hysterectomy. Intraoperatively, bilateral ureteral stents were placed due to ureteral distortion. History was also notable for CKD G2A3. Prior renal biopsy showed hypertensive damage and monotypic IgA Kappa mesangial deposits suggestive of PGNMID, with negative hematologic work up.
She presented with baseline creatinine of 0.9 mg/dL briefly rising to 1.0-1.1 mg/dL post-op. Admission blood pressure was ~180/110 mm Hg compared to home baseline of 160/90 mm Hg. After initial improvement on oral labetalol, systolic blood pressure rose to 180 mm Hg on post-op day 4, prompting pre-eclampsia concerns. She received 6g IV magnesium sulfate and started a 2g/hr infusion. Labetalol was doubled, amlodipine was added, and pain improved with blood pressure dropping to a sustained 90/50 mm Hg.
The next morning, serum magnesium was 10.0 mg/dL and serum potassium was 6.4 mmol/L with ongoing hypotension and new somnolence. Aside from constipation, no other cause for hyperkalemia was identified beyond magnesium (no AKI, acidemia, urinary obstruction, dietary sources or medications). Magnesium normalized to 2.2 mg/dL within 48 hours of stopping the infusion, despite a dose of milk of magnesia. Potassium remained 5.4-5.7 mmmol/L for two days, with good urine output on diuretics and potassium binders. During this time, she had refractory constipation and a brief non-oliguric AKI to creatinine of 1.5 mg/dL, likely prerenal due to hypotension and somnolence-induced poor oral intake. By discharge, electrolytes normalized, constipation and AKI resolved, and ureteral stents were removed. She has been lost to follow up.
Discussion
Although hypomagnesemia-induced hypokalemia via loss of ROMK inhibition is well known, reports of the reverse are rare. This case highlights the multi-mechanistic vicious cycle between hypermagnesemia and hyperkalemia. In addition to ROMK inhibition, constipation increases potassium and magnesium absorption. Further, hypotension and somnolence can worsen AKI. Even mild CKD is a critical risk factor for iatrogenic hypermagnesemia. Symptoms are nonspecific and require close monitoring and high index of suspicion.