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Iron deficiency (ID) is the most common micronutrient deficiency in pregnancy, especially impacting medically underserved populations worldwide. Iron deficiency (ID) in pregnancy predisposes neonates to poor iron status, i.e., congenital ID and associated adverse effects. The role of congenital ID on human kidney development is unstudied, but impaired fetal kidney development is possible. Both vascular and global nutrient restriction rat models report impaired fetal kidney development, as well as induce hypertension, supporting the developmental origins of health and disease (DOHaD) hypothesis. This review compiles findings from 17 published studies in rats examining congenital or early postnatal ID, showing the same. The review compares histological and physiological findings in both congenital and postnatal ID, placing these in the context of recent knowledge describing molecular mechanistic pathways regulating nephrogenesis. Findings in rat early-life ID include lower kidney iron levels, lower glomerular generations and estimated glomerular numbers, larger maculae densa size, interstitial fibrosis, and prolonging active glomerulogenesis past normal temporal cessation. Additionally, several physiological studies in rat congenital ID promote altered renin\u2013angiotensin signaling and hypertension with maturation, especially in males. Key findings of morphological kidney maldevelopment, altered renin\u2013angiotensin signaling, and hypertension in early-life ID underscore the urgent need for future mechanistic data in animals such as rats. The long-term goal would be to leverage understanding from these data into either preventative or early therapeutic strategies in children.<\/jats:p>\n                  <jats:p>\n                    <jats:bold>Graphical Abstract<\/jats:bold>\n                  <\/jats:p>","DOI":"10.1007\/s00467-025-06762-w","type":"journal-article","created":{"date-parts":[[2025,4,12]],"date-time":"2025-04-12T04:02:48Z","timestamp":1744430568000},"page":"23-32","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Developmental origins of disease \u2013 Effects of iron deficiency in the rat developing kidney and beyond"],"prefix":"10.1007","volume":"41","author":[{"given":"Anthony","family":"Babu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5228-6501","authenticated-orcid":false,"given":"Whitley N.","family":"Hulse","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5493-3269","authenticated-orcid":false,"given":"Matthew W.","family":"Harer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9355-5202","authenticated-orcid":false,"given":"Keri A.","family":"Drake","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6098-2646","authenticated-orcid":false,"given":"Pamela J.","family":"Kling","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,4,12]]},"reference":[{"key":"6762_CR1","doi-asserted-by":"publisher","first-page":"54","DOI":"10.1016\/j.siny.2006.10.007","volume":"12","author":"R Rao","year":"2007","unstructured":"Rao R, Georgieff MK (2007) Iron in fetal and neonatal nutrition. 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