Kim Kyeong Min, Kwon Soon Kil, Kim Hye-Young
Department of Internal Medicine, Eulji University Hospital, Eulji University College of Medicine, Daejeon, Korea.
Department of Internal Medicine, Chungbuk National University Hospital, Chungbuk National University College of Medicine, Cheongju, Korea.
Electrolyte Blood Press. 2016 Dec;14(2):35-37. doi: 10.5049/EBP.2016.14.2.35. Epub 2016 Dec 31.
Familial renal glycosuria (FRG) is an inherited disorder characterized by persistent glycosuria in the absence of hyperglycemia. It is caused by mutations in the sodium-glucose co-transporter, leading to increase in the renal excretion of glucose and sodium. However, there have been no studies on the role of fasting and postprandial changes in the urinary sodium excretion in patients with FRG. We report a case of renal glycosuria, which was confirmed by a mutation via gene sequencing, and compared the postprandial urinary glucose and sodium excretion. A 26-year-old man sometimes experienced glycosuria on routine screening; however, other laboratory findings were normal. His fasting and postprandial urinary glucose excretion levels were 295mg/dL and 2,170mg/dL, respectively. The fasting and postprandial urinary sodium excretion levels were 200mEq/L and 89mEq/L, respectively. In patients with FRG, excessive diuresis might be prevented by a compensatory mechanism that reduces postprandial sodium excretion.
家族性肾性糖尿（FRG）是一种遗传性疾病，其特征是在无高血糖的情况下持续出现糖尿。它由钠-葡萄糖共转运体的突变引起，导致肾脏对葡萄糖和钠的排泄增加。然而，尚未有关于FRG患者空腹和餐后尿钠排泄变化作用的研究。我们报告一例经基因测序突变确诊的肾性糖尿病例，并比较了餐后尿葡萄糖和钠排泄情况。一名26岁男性在常规筛查时有时出现糖尿；然而，其他实验室检查结果正常。他的空腹和餐后尿葡萄糖排泄水平分别为295mg/dL和2170mg/dL。空腹和餐后尿钠排泄水平分别为200mEq/L和89mEq/L。在FRG患者中，可能通过减少餐后钠排泄的代偿机制来预防过度利尿。
