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Developmental Origins of Kidney Disease: Renal Programming

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 December 2025 | Viewed by 537

Special Issue Editor


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Guest Editor
Department of Pediatrics, Korea University College of Meicine, 73, Goryeodae-ro, Seongbuk-gu, Seoul, Republic of Korea
Interests: air pollution; chronic kidney disease; congenital anomalies of kidney and urinary tract; renal development; renal programming; renin angiotensin system

Special Issue Information

Dear Colleagues,

Adverse environmental exposures during early life—including the fetal and perinatal periods—can profoundly disrupt normal developmental trajectories, thereby increasing the susceptibility to chronic diseases in adulthood, such as chronic kidney disease. Numerous studies have investigated the consequences of suboptimal intrauterine environments, including maternal dietary imbalances, maternal diabetes, exposure to glucocorticoids or environmental toxicants, including fine particles, and placental insufficiency. These investigations have consistently demonstrated impairments in renal morphogenesis, reduced nephron endowment, and the dysregulation of key genes as well as signaling pathways that govern kidney development, postnatal growth, and the progression of renal disease in offspring.

This Special Issue aims to feature high-quality original research articles and comprehensive reviews that advance our understanding of the molecular mechanisms underlying renal programming as well as novel therapeutic approaches to renal reprogramming. We particularly welcome studies offering mechanistic insights at the molecular and cellular levels.

Dr. Hyung-Eun Yim
Guest Editor

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Keywords

  • air pollution
  • chronic kidney disease
  • congenital anomalies of the kidneys and urinary tract
  • high-risk pregnancy
  • nephrogenesis
  • renal programming
  • renin angiotensin system

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Published Papers (1 paper)

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Review

22 pages, 1469 KB  
Review
Maternal Separation and Negative Renal Programming, Evidence of Morphofunctional Alterations in Rodent Models: Systematic Review and Meta-Analysis
by Jhonatan Duque-Colorado, Josue Rivadeneira and Bélgica Vásquez
Int. J. Mol. Sci. 2025, 26(21), 10509; https://doi.org/10.3390/ijms262110509 - 29 Oct 2025
Viewed by 385
Abstract
Exposure to stress during early developmental stages correlates with persistent alterations in multiple physiological systems, including the renal system. In rodents, maternal separation (MS) is a widely used experimental model to simulate postnatal adversity. Although this condition affects various renal parameters, a gap [...] Read more.
Exposure to stress during early developmental stages correlates with persistent alterations in multiple physiological systems, including the renal system. In rodents, maternal separation (MS) is a widely used experimental model to simulate postnatal adversity. Although this condition affects various renal parameters, a gap persists in knowledge regarding its impact on the functional unit of the kidney and the organization of the parenchyma. Thus, the objective of this systematic review was to analyze the effects of MS on the morphofunctional characteristics of the kidney in rodent models. We developed a protocol a priori following the SYRCLE and PRISMA guidelines and registered it in PROSPERO (CRD420251004703). We searched Web of Science, Scopus, Medline, Embase, BIREME-BVS, and SciELO without language or date restrictions, targeting experimental studies in rodents subjected to MS that evaluated structural, functional, or molecular alterations. Three independent reviewers performed data selection and extraction, and they assessed the risk of bias using the SYRCLE’s RoB tool. We included seven studies that met the eligibility criteria. At the structural level, studies reported cellular infiltrates positive for MPO, CD44, and TLR4, along with increased cortical and medullary microvascular density. Regarding renal function, the included studies described changes in ACE1 and ACE2 activity, oxidative stress, and enzymatic imbalance accompanied by a compensatory antioxidant response. At the molecular level, the studies reported variations in the expression of adrenergic receptors and the renin-angiotensin system. These findings suggest that MS may compromise the organization and functional integrity of the developing kidney, underscoring the need for studies that integrate structural and functional analyses in greater depth. Full article
(This article belongs to the Special Issue Developmental Origins of Kidney Disease: Renal Programming)
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