Renal dysplasia development and chronic kidney disease
- PMID: 40000855
- DOI: 10.1038/s41390-025-03950-0
Renal dysplasia development and chronic kidney disease
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.
© 2025. The Author(s), under exclusive licence to the International Pediatric Research Foundation, Inc.
Conflict of interest statement
Competing interests: All authors certify that they have no financial and/or personal relationship with any person or organization that could have inappropriately influenced their work. The authors declare no conflicts of interest. Consent statement: This review article does not involve any new studies with human participants or animals performed by any of the authors. All data cited in this review are from published studies, and appropriate consent statements are available in the original publications.
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