Renal glucosuria in children.

Meral Torun Bayram, Salih Kavukcu
{"title":"Renal glucosuria in children.","authors":"Meral Torun Bayram, Salih Kavukcu","doi":"10.5409/wjcp.v14.i1.91622","DOIUrl":null,"url":null,"abstract":"<p><p>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 <i>sodium/glucose cotransporter 5A2</i> 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.</p>","PeriodicalId":75338,"journal":{"name":"World journal of clinical pediatrics","volume":"14 1","pages":"91622"},"PeriodicalIF":0.0000,"publicationDate":"2025-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11686576/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"World journal of clinical pediatrics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5409/wjcp.v14.i1.91622","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

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.

儿童肾性糖尿症。
肾脏在维持葡萄糖稳态中起着至关重要的作用。在正常的肾小管功能下,大部分从肾小球滤出的葡萄糖被近端肾小管重新吸收,仅在尿液中留下微量。糖尿可作为全身性近端肾小管功能障碍的症状或当重吸收阈值超过或葡萄糖阈值降低时发生,如家族性肾性糖尿症(FRG)。尽管血糖水平和肾小管功能正常,但FRG的特征是持续的糖尿,主要与钠/葡萄糖共转运蛋白5A2基因突变有关,该基因编码钠-葡萄糖共转运蛋白(SGLT) 2。抑制sglt已被提出作为一种新的糖尿病治疗策略,由于FRG通常被认为是一种无症状和良性的疾病,它激发了使用SGLT2抑制剂治疗2型糖尿病的临床前和临床研究。然而,FRG患者可能表现出体重或身高较低、全身血压改变、尿布性皮炎、氨基酸尿、血清尿酸水平降低和高钙尿等临床特征。对肾性高血糖的病理生理、分子遗传学、临床表现等方面的认识有待进一步研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
3.20
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信