Journal of nephrology · 2026
Dapagliflozin corrects hypomagnesemia in kidney-transplant patients.
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Guillot Douchka, Dejoie Thomas, Kerleau Clarisse, Walencik Alexandre, Dantal Jacques, Maillard Clémence, Legouis David, Figueres Lucile
Аннотация
BACKGROUND: Hypomagnesemia frequently occurs after kidney transplantation, potentially contributing to morbidity. Sodium-glucose co-transporter 2 inhibitors (SGLT2i), such as dapagliflozin, have proven benefits in chronic kidney disease, but their effects on serum magnesium in non-diabetic transplant recipients remain unclear.
METHODS: We retrospectively studied 122 adult kidney-transplant recipients who initiated dapagliflozin between September 2020 and July 2023. We obtained two serum samples: one before and one after dapagliflozin initiation in 94 patients. After excluding patients with inadequate sampling or early discontinuation, 34 patients were analyzed and compared with 96 controls not receiving dapagliflozin.
RESULTS: At baseline, hypomagnesemia was present in 26.5% of dapagliflozin-treated patients and 22.9% of controls. After a median of 8.1 months on dapagliflozin, serum magnesium increased significantly (P = .00018), correcting hypomagnesemia in 7 of 9 affected patients. No significant change occurred in the control group. Serum phosphate also significantly increased (P = .026), while estimated glomerular filtration rate (eGFR) declined (P = .0001), consistent with known hemodynamic effects of SGLT2i. No significant variations in magnesium, phosphate, or eGFR were observed among controls.
CONCLUSIONS: In this cohort, dapagliflozin use was associated with improved serum magnesium in kidney-transplant recipients, particularly those with baseline hypomagnesemia, thus warranting further prospective investigation.
METHODS: We retrospectively studied 122 adult kidney-transplant recipients who initiated dapagliflozin between September 2020 and July 2023. We obtained two serum samples: one before and one after dapagliflozin initiation in 94 patients. After excluding patients with inadequate sampling or early discontinuation, 34 patients were analyzed and compared with 96 controls not receiving dapagliflozin.
RESULTS: At baseline, hypomagnesemia was present in 26.5% of dapagliflozin-treated patients and 22.9% of controls. After a median of 8.1 months on dapagliflozin, serum magnesium increased significantly (P = .00018), correcting hypomagnesemia in 7 of 9 affected patients. No significant change occurred in the control group. Serum phosphate also significantly increased (P = .026), while estimated glomerular filtration rate (eGFR) declined (P = .0001), consistent with known hemodynamic effects of SGLT2i. No significant variations in magnesium, phosphate, or eGFR were observed among controls.
CONCLUSIONS: In this cohort, dapagliflozin use was associated with improved serum magnesium in kidney-transplant recipients, particularly those with baseline hypomagnesemia, thus warranting further prospective investigation.