SUN-607 - When Oral Magnesium Fails: A Novel Strategy for Renal Magnesium Wasting in Type 1 Diabetes

Hypomagnesemia is common in diabetes mellitus (DM) and may be exacerbated by renal magnesium wasting, particularly in the setting of poor glycemic control and tubular injury. Management is challenging when oral magnesium supplementation is ineffective or poorly tolerated, and evidence guiding adjunctive pharmacologic strategies remains limited.

We report a 24 y/o male with T1DM complicated by neuropathy who, over the course of one year, experienced recurrent hospitalizations for severe hypomagnesemia associated with torsades de pointes, orthostatic symptoms, palpitations, and myasthenia. Laboratory evaluation demonstrated persistent hypomagnesemia with a spot urine magnesium level of 14.9 mg/dL and a fractional excretion of magnesium of 13% (normal < 4%), consistent with renal magnesium wasting. Genetic testing for inherited magnesium-wasting tubulopathies was negative. Microalbuminuria suggested early diabetic kidney involvement. After exclusion of medication-related and gastrointestinal (GI) causes, hypomagnesemia was attributed to acquired renal magnesium wasting related to osmotic diuresis and insulin resistance–mediated impairment of tubular magnesium reabsorption.
Multiple high-dose oral magnesium formulations (oxide 400 mg TID, chloride 520 mg TID, lactate 84 mg BID, glycinate 400 mg TID, and combination products) were attempted but were limited by significant GI intolerance, necessitating frequent IV magnesium repletion. Serum magnesium levels declined when IV therapy was withheld.

The patient was initiated on amiloride 10 mg daily to reduce distal tubular magnesium wasting and was counseled on hydration and a high-magnesium diet. Despite this, he was readmitted one month later with recurrent severe hypomagnesemia. Given persistent renal magnesium losses, empagliflozin was cautiously initiated for its magnesium-conserving effects, with close monitoring for ketoacidosis. Oral magnesium supplementation was simplified and titrated using divided doses of citrate, glycinate, and chloride. On follow-up, the patient achieved stable serum magnesium levels (>1.7 mg/dL), remained asymptomatic, and experienced no further arrhythmias or hospitalizations, without development of diabetic ketoacidosis.

This case underscores the complexity of refractory hypomagnesemia in patients with T1DM and renal magnesium wasting. The combination of amiloride, adjunctive SGLT2 inhibition, and individualized oral supplementation may be effective when conventional replacement fails.This approach should be considered on a case-by-case basis with careful monitoring. Further investigation is warranted to better define magnesium-conserving pharmacologic approaches for renal magnesium wasting in patients with DM.

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