A Case of Isolated Glycosuria Mediated by an SLC5A2 Gene Mutation and Characterized by Postprandial Heavy Glycosuria Without Salt Wasting.
- Author:
Kyeong Min KIM
1
;
Soon Kil KWON
;
Hye Young KIM
Author Information
- Publication Type:Case Report
- Keywords: Renal glycosuria; Sodium glucose cotransporters; Renal excretion
- MeSH: Adult; Diuresis; Fasting; Glucose; Glycosuria*; Glycosuria, Renal; Humans; Hyperglycemia; Mass Screening; Renal Elimination; Sodium; Sodium-Glucose Transport Proteins
- From:Electrolytes & Blood Pressure 2016;14(2):35-37
- CountryRepublic of Korea
- Language:English
- Abstract: 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 SLC5A2 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.
