Li Zhang, Chunjiang Yang, Xing Liu, Dawei He, Tao Lin, Yuanyuan Zhang, Guanghui Wei, Deying Zhang
{"title":"Renal dysplasia development and chronic kidney disease.","authors":"Li Zhang, Chunjiang Yang, Xing Liu, Dawei He, Tao Lin, Yuanyuan Zhang, Guanghui Wei, Deying Zhang","doi":"10.1038/s41390-025-03950-0","DOIUrl":null,"url":null,"abstract":"<p><p>Renal dysplasia is a common congenital birth defect in childhood, caused by fetal genetic defects, epigenetic modification disorders, or environmental factors. Maternal malnutrition, placental insufficiency, and exposure to harmful substances such as alcohol, angiotensin-converting enzyme inhibitors, and cocaine during pregnancy increase the risk of fetal renal dysplasia. The pathogenesis of this disease involves abnormal formation of renal units, leading to structural and functional abnormalities of the kidney. If left untreated, renal dysplasia can progress to chronic kidney disease (CKD) in children. This review explores the etiology and pathogenesis of renal dysplasia, emphasizing the intrinsic link between renal dysplasia and CKD through various pathological pathways. Additionally, we propose potential therapeutic agents targeting these mechanisms. We also highlight future research directions to further understand and address this issue. We hope this review will deepen clinicians' understanding of renal dysplasia and promote further laboratory research in this area. IMPACT: 1. This review comprehensively summarizes and elucidates the complex relationship between renal dysplasia and chronic kidney disease (CKD) based on previous research, offering new directions for related studies. 2. It expands upon conservative treatment approaches for renal dysplasia, providing more clinical options for therapeutic intervention.</p>","PeriodicalId":19829,"journal":{"name":"Pediatric Research","volume":" ","pages":""},"PeriodicalIF":3.1000,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pediatric Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41390-025-03950-0","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PEDIATRICS","Score":null,"Total":0}
引用次数: 0
Abstract
Renal dysplasia is a common congenital birth defect in childhood, caused by fetal genetic defects, epigenetic modification disorders, or environmental factors. Maternal malnutrition, placental insufficiency, and exposure to harmful substances such as alcohol, angiotensin-converting enzyme inhibitors, and cocaine during pregnancy increase the risk of fetal renal dysplasia. The pathogenesis of this disease involves abnormal formation of renal units, leading to structural and functional abnormalities of the kidney. If left untreated, renal dysplasia can progress to chronic kidney disease (CKD) in children. This review explores the etiology and pathogenesis of renal dysplasia, emphasizing the intrinsic link between renal dysplasia and CKD through various pathological pathways. Additionally, we propose potential therapeutic agents targeting these mechanisms. We also highlight future research directions to further understand and address this issue. We hope this review will deepen clinicians' understanding of renal dysplasia and promote further laboratory research in this area. IMPACT: 1. This review comprehensively summarizes and elucidates the complex relationship between renal dysplasia and chronic kidney disease (CKD) based on previous research, offering new directions for related studies. 2. It expands upon conservative treatment approaches for renal dysplasia, providing more clinical options for therapeutic intervention.
期刊介绍:
Pediatric Research publishes original papers, invited reviews, and commentaries on the etiologies of children''s diseases and
disorders of development, extending from molecular biology to epidemiology. Use of model organisms and in vitro techniques
relevant to developmental biology and medicine are acceptable, as are translational human studies