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We previously showed that male preterm mice with diabetes develop early features of DKD, including reduced podocyte density, decreased renin expression, activation of angiogenesis pathways, and impaired endothelial\u2013podocyte signaling. Here, we examine whether preterm birth similarly accelerates DKD progression in female mice and compare structural and transcriptomic outcomes in the females to the prior male cohort to assess sex\u2010specific differences.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Preterm mice were delivered by Caesarean section at 19\u2009days post conception (dpc) and term mice at 20 dpc. Hyperglycemia was induced at 6\u2009weeks with streptozotocin to generate term\u2010diabetic (T\u2010D) and preterm\u2010diabetic (PT\u2010D) groups; controls were term\u2010nondiabetic (T\u2010ND) and preterm\u2010nondiabetic (PT\u2010ND). Body weight and glucose were monitored, and kidneys were analyzed at 18\u2009weeks using histologic, stereologic, imaging, and transcriptomic methods.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Compared with T\u2010ND females, PT\u2010D females showed higher albuminuria, more atubular glomeruli, reduced proximal tubule (PT) fraction, and pro\u2010fibrotic gene activation. Compared to T\u2010D females, PT\u2010D females had higher blood urea nitrogen (BUN) levels and reduced PT fraction. This was associated with activation of pathways associated with the vasculature and suppression of mitochondrial metabolism gene pathways, along with Notch signalling alterations. Sex differences included a lower PT fraction in preterm females than males and fewer atubular glomeruli in PT\u2010D females than PT\u2010D males. Renin expression was lower in PT\u2010D than T\u2010D in males only. When comparing PT\u2010D to T\u2010D across sexes, 582 differentially expressed genes were unique to females. Notch signalling was upregulated in both male and female PT\u2010D mice compared to T\u2010D.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Preterm birth increases susceptibility to kidney injury in females after exposure to hyperglycemia. However, preterm females with hyperglycemia are more resistant to kidney damage than males.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/edm2.70223","type":"journal-article","created":{"date-parts":[[2026,4,20]],"date-time":"2026-04-20T20:10:56Z","timestamp":1776715856000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Preterm Birth Increases Susceptibility to Hyperglycemia\u2010Induced Kidney Injury With Sex\u2010Specific Differences in Structural and Molecular Responses"],"prefix":"10.1002","volume":"9","author":[{"given":"Rachel K.","family":"Dailey","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Pediatrics University of Virginia  Charlottesville Virginia USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aleksandra","family":"Cwiek","sequence":"additional","affiliation":[{"name":"Department of Cell Biology University of Virginia  Charlottesville 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