Minireviews
Copyright ©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
Renal glucosuria in children
Meral Torun Bayram, Salih Kavukcu
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.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
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
Abstract

The kidneys play a critical role in maintaining glucose homeostasis. Under normal renal tubular function, most of the glucose filtered from the glomeruli is reabsorbed in the proximal tubules, leaving only trace amounts in the urine. Glycosuria can occur as a symptom of generalized proximal tubular dysfunction or when the reabsorption threshold is exceeded or the glucose threshold is reduced, as seen in familial renal glycosuria (FRG). FRG is characterized by persistent glycosuria despite normal blood glucose levels and tubular function and is primarily associated with mutations in the sodium/glucose cotransporter 5A2 gene, which encodes the sodium-glucose cotransporter (SGLT) 2. Inhibiting SGLTs has been proposed as a novel treatment strategy for diabetes, and since FRG is often considered an asymptomatic and benign condition, it has inspired preclinical and clinical studies using SGLT2 inhibitors in type 2 diabetes. However, patients with FRG may exhibit clinical features such as lower body weight or height, altered systemic blood pressure, diaper dermatitis, aminoaciduria, decreased serum uric acid levels, and hypercalciuria. Further research is needed to fully understand the pathophysiology, molecular genetics, and clinical manifestations of renal glucosuria.

Keywords: Sodium-glucose cotransporters; Basolateral glucose transporters; Familial renal glucosuria; Intestinal glucose-galactose malabsorption; Fanconi-Bickel syndrome; Sodium-glucose cotransporter 2 inhibitors

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.