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Abstract: PO1130

Severe Hypermagnesemia: A Potential Cause of Acute Hyperkalemia

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Nahapetyan, Lusine, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, United States
  • Prakash-Polet, Sindhuri, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, United States
  • Rosen, Raphael Judah, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, United States
  • Han, Heedeok, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, United States
Introduction

Hypermagnesemia is not a well-established cause of hyperkalemia. In this case report we explore the association of acute hypermagnesemia and hyperkalemia.

Case Description

30 year old female G1P0 with chronic HTN since age 26, CACUT was admitted for preeclampsia with severe features (new proteinuria 5.5 g/24h, AKI (cr peaked at 1.33 from baseline 0.65), HTN, LE edema). Patient delivered via C-section at 27 weeks 6 days. Extensive AKI work-up was negative. At admission had normal K 4.4, Na 143, Ca 8.6 (albumin 3.4), bicarb 21, cr 0.96, LDH 213, glucose 111, Hb 10, Plt 177, renin 1.39, aldosterone 13.6.
At admission, she was started on Mg sulfate infusion for seizure prophylaxis. After patient’s serum Mg acutely increased (peak 8), she simultaneously developed acute hyperkalemia (peak K 6.1, bicarb 19, cr 1.1, normal EKG). Hyperkalemia improved to 5.3 with IV Lasix, bicarbonate, and NS but persisted until Mg infusion was discontinued and Mg levels normalized to 2.5 leading to normalization of K (4.3).

Only two previous case studies have described a potential association between hypermagnesemia and hyperkalemia. We described a case when acute hypermagnesemia led to acute hyperkalemia, which persisted until Mg levels normalized. There were no other etiologies of hyperkalemia in this case (AKI was not severe to lead to hyperkalemia; patient was on beta-blocker but this was a chronic medication; no other medications known to cause hyperkalemia; normal aldosterone, no significant change in bicarb).

Discussion

Magnesium plays an important role in potassium homeostasis in kidney and intestines. One possible mechanism is that cytoplasmic magnesium concentration has a profound effect on ROMK potassium channels (expressed in the thick ascending and cortical collecting tubules); a high intracellular Mg concentration blocks channel activity. Additionally, ROMK is an important pathway for potassium secretion in the distal nephron. Therefore, potassium levels should be closely monitored in patients who receive high dose magnesium infusions and are at high risk of hypermagnesemia and subsequent hyperkalemia.