Van Laecke Steven, Caluwe Rogier, Huybrechts Inge, Nagler Evi V, Vanholder Raymond, Peeters Patrick, Van Vlem Bruno, Van Biesen Wim
Renal Division, Department of Internal Medicine, Ghent University Hospital, Ghent, Belgium.
Renal Division, Onze-Lieve-Vrouwziekenhuis (OLV) Hospital, Aalst, Belgium.
Ann Transplant. 2017 Aug 29;22:524-531. doi: 10.12659/aot.903439.
BACKGROUND Hypomagnesemia is associated with a disturbed glucose metabolism. Insulin hypo-secretion predicts diabetes in the general population and in transplant recipients. We aimed to assess whether magnesium improves insulin secretion and glycemic control after transplantation in prevalent hypomagnesemic kidney transplant recipients. MATERIAL AND METHODS We conducted an open-label, randomized, parallel-group study. Eligible participants were adults more than 4 months after kidney transplantation on tacrolimus with persisting serum magnesium concentrations <1.8 mg/dL randomized to magnesium oxide supplementation up to a maximum of 3 times 450 mg daily (N=26) or no supplements (N=26). Insulin secretion was assessed by OGTT-derived, first-phase insulin secretion (FPIR). The primary endpoint was the mean difference in FPIR between baseline and 6 months after randomization. Secondary endpoints were differences in HbA1c and insulin resistance, measured by HOMA. Dietary magnesium was assessed by a food-frequency questionnaire. All analyses were done on an intention-to-treat basis. RESULTS Magnesium with a mean daily dose of 688±237mg in the treatment group failed to lead to significant differences between the 2 groups in FPIR, fasting glucose, HbA1c, or HOMA-IR. Persisting hypomagnesemia was very common and associated with more insulin hypo-secretion, glucose intolerance, and lower dietary magnesium intake (142±56 versus 202±90 mg; p=0.015) as compared to patients with a rise in serum magnesium over 6 months. CONCLUSIONS Magnesium supplementation does not improve insulin secretion in stable hypomagnesemic kidney transplant recipients on tacrolimus. Persisting hypomagnesemia is associated with impaired glucose tolerance, insulin hypo-secretion, and dietary factors.
低镁血症与糖代谢紊乱有关。胰岛素分泌不足在普通人群和移植受者中都预示着糖尿病。我们旨在评估在患有低镁血症的肾移植受者中，镁是否能改善移植后的胰岛素分泌和血糖控制。材料与方法：我们进行了一项开放标签、随机、平行组研究。符合条件的参与者为肾移植术后4个月以上、服用他克莫司且血清镁浓度持续低于1.8mg/dL的成年人，随机分为氧化镁补充组，每日最大剂量为3次450mg（N = 26）或不补充组（N = 26）。通过口服葡萄糖耐量试验（OGTT）得出的第一相胰岛素分泌（FPIR）评估胰岛素分泌。主要终点是随机分组后基线与6个月时FPIR的平均差异。次要终点是糖化血红蛋白（HbA1c）和胰岛素抵抗的差异，通过稳态模型评估（HOMA）。通过食物频率问卷评估膳食镁摄入量。所有分析均基于意向性分析。结果：治疗组平均每日剂量为688±237mg的镁未能使两组在FPIR、空腹血糖、HbA1c或HOMA-IR方面产生显著差异。持续性低镁血症非常常见，与胰岛素分泌不足、葡萄糖耐量异常以及较低的膳食镁摄入量（142±56对202±90mg；p = 0.015）相关，而血清镁在6个月内升高的患者则不然。结论：在服用他克莫司的稳定低镁血症肾移植受者中，补充镁并不能改善胰岛素分泌。持续性低镁血症与葡萄糖耐量受损、胰岛素分泌不足和饮食因素有关。
