©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Pediatr. Mar 9, 2025; 14(1): 91622
Published online Mar 9, 2025. doi: 10.5409/wjcp.v14.i1.91622
Published online Mar 9, 2025. doi: 10.5409/wjcp.v14.i1.91622
Renal glucosuria in children
Meral Torun Bayram, Salih Kavukcu, Division of Nephrology, Department of Pediatrics, Dokuz Eylül University, School of Medicine, Inciralti-Balcova 35340, Izmir, Türkiye
Author contributions: Both authors contributed equally to this review, and both have read and approved the final version of the manuscript to be published.
Conflict-of-interest statement: All authors declare no conflict of interest in publishing the manuscript.
Corresponding author: Meral Torun Bayram, Doctor, Professor, Division of Nephrology, Department of Pediatrics, Dokuz Eylül University, School of Medicine, 15 July Medicine and Art Campus, Inciralti-Balcova 35340, Izmir, Türkiye. meralt.bayram@yahoo.com.tr
Received: December 31, 2023
Revised: October 10, 2024
Accepted: November 13, 2024
Published online: March 9, 2025
Processing time: 354 Days and 10.8 Hours
Revised: October 10, 2024
Accepted: November 13, 2024
Published online: March 9, 2025
Processing time: 354 Days and 10.8 Hours
Core Tip
Core Tip: Familial renal glucosuria (FRG) is the most common inherited defect in renal glucose transport. Mutations in the sodium/glucose cotransporter 5A2 gene, which encodes sodium-glucose cotransporter (SGLT) 2, lead to FRG. Although generally considered a benign condition, FRG has inspired pharmacological interest, especially as SGLT2 inhibitors have become a therapeutic target for reducing hyperglycemia in type 2 diabetes. The glucose-lowering mechanism of SGLT2 inhibitors closely resembles the pathophysiology of renal glucosuria. Detailed clinical and laboratory examinations of patients with FRG could provide further insights into the complications, significance, and long-term outcomes of SGLT2 inhibitor therapy.