{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T20:30:14Z","timestamp":1786480214571,"version":"build-2736575974"},"reference-count":145,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T00:00:00Z","timestamp":1771286400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Transferrin receptor 1 is critical for perinatal nephron growth and maturation; its deletion results in widespread cystic hypodysplasia.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Nontransferrin bound iron traffic is a physiologic source of iron in the midgestation embryo and complements transferrin receptor 1.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Cystic hypodysplasia can be rescued by exogenous iron or by the activation of systemic iron traffic with hypoxia inducible factor activators.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Periconceptual maternal iron deficiency (FeD) is a worldwide cause of premature births and low birth weights. Yet, it is unknown whether FeD affects all developing tissues equally or rather target-\n                      <jats:italic toggle=\"yes\">s<\/jats:italic>\n                      pecific lineages. In addition, since FeD restricts both transferrin bound and nontransferrin bound iron species, their unique contributions to organogenesis are indeterminant.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To address questions of iron traffic and kidney development, we examined the deletion of the singular transferrin receptor (\n                      <jats:italic toggle=\"yes\">TfR1\u2212\/\u2212<\/jats:italic>\n                      ), created green flourescent protein-labeled\n                      <jats:italic toggle=\"yes\">TfR1\u2212\/\u2212<\/jats:italic>\n                      embryonic stem cells for inoculation into wild blastocysts, and created\n                      <jats:italic toggle=\"yes\">TfR1<\/jats:italic>\n                      -floxed mice to generate cell autonomous deletions of\n                      <jats:italic toggle=\"yes\">TfR1<\/jats:italic>\n                      in mesenchymal, ureteric, and stromal derivatives. Finally, we created a model of global FeD with iron poor diets, for comparison with cell autonomous\n                      <jats:italic toggle=\"yes\">TfR1<\/jats:italic>\n                      deletions.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Transferrin receptor deletions only modestly suppressed tubulogenesis, had little, if any effect on the growth of the ureteric bud and no gross effects on kidney stroma at mid gestation. By contrast, nutritional FeD nearly abolished kidney development, highlighting the limited phenotypes induced by transferrin receptor deletion. Yet, in the second postnatal week, the critical function of\n                      <jats:italic toggle=\"yes\">TfR1<\/jats:italic>\n                      became evident by the growth of residual\n                      <jats:italic toggle=\"yes\">TfR1+<\/jats:italic>\n                      cells that had escaped Cre-mediated deletion and by tubular segment-specific polycystic transformation. Timed treatment with iron or systemic activators of iron trafficking prevented both cystic dysplasia and the terminal loss of kidney function, reversing extensive malformations of the kidney.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">TfR1<\/jats:italic>\n                      is the critical iron species targeting postnatal tubulogenesis, but in the embryo,\n                      <jats:italic toggle=\"yes\">TfR1<\/jats:italic>\n                      must be complemented by alternative iron species called nontransferrin bound iron. Iron-deficient kidney disease is reversible postnatally.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.34067\/kid.0000001064","type":"journal-article","created":{"date-parts":[[2026,2,17]],"date-time":"2026-02-17T17:00:49Z","timestamp":1771347649000},"page":"982-1002","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":1,"title":["A Switch in Iron Delivery Is Critical for Postnatal Kidney Development"],"prefix":"10.34067","volume":"7","author":[{"given":"Andong","family":"Qiu","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Columbia University, New York, New York"},{"name":"School of Life Sciences and Biotechnology, Advanced Institute for Translational Medicine, Tongji University, Shanghai, 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Department of Medicine, Columbia University, New York, New York"},{"name":"Department of Radiology, University of Washington, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-4553-207X","authenticated-orcid":false,"given":"Andrew","family":"Yaeh","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Columbia University, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1352-0115","authenticated-orcid":false,"given":"Beatriz Desanti","family":"de Oliveira","sequence":"additional","affiliation":[{"name":"Division of General Medicine, Department of Medicine, Columbia University, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8442-0640","authenticated-orcid":false,"given":"Roger 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