#2449 Treatment of chronic hypomagnesemia with SGLT2-inhibitor in a patient with Gitelman syndrome—a case report
Abstract
Gitelman syndrome is an inherited distal tubulopathy with low potassium and magnesium levels. The magnesium supplementation has great limitations in the patients because of its side effects.
The inhibitors of the sodium-glucose-cotransporter-2 (SGLT2) can help magnesium-sparing, independently from the distal tubules. Therefore, SGLT2-inhibitors may also increase magnesium levels in patients with Gitelman syndrome. This hypothesis was examined in a patient with Gitelman syndrome (proven with genetic test), who had symptomatic hypomagnesemia with the highest dose of tolerable supplementation. The patient had no other indications for the use of SGLT2-inhibitors.
After the informed consent of the 38-year-old female patient, a request for medication use beyond its indication was sent to the National Center for Public Health and Pharmacy. After the approval, the patient started on empagliflozin 10 mg therapy with the same salt-supplementation. Laboratory tests were conducted before the initiation of the treatment and after two weeks.
Serum creatinine levels rose (56 vs. 65 umol/L) but kidney function remained stable (creatinine clearance 129 vs. 127 ml/min) after initiation of the therapy. Proteinuria became lower (240 vs. 216 mg/day, urinary albumin/creatinine ratio 1.2 vs. 0.9 mg/mmol). The urinary excretion of sodium was more (261 vs. 325 mmol/day) but the serum sodium level was stable (137 vs. 137 mmol/L). The rise of the chloride excretion (350 vs. 479 mmol/day) did not…
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