Renal Adaptation in Gestational Iron Deficiency

Background Severe gestational iron deficiency (ID) can impair fetal growth and renal development, ultimately causing adult hypertension. Nephrogenesis continues until P7 in rats. Our aim was to examine rat kidney adaptations during gestational ID. Methods From gestational day 2 to postnatal day (P)7, pregnant rats were fed IS iron sufficient (198 mg Fe/kg diet) or ID rat diet (<6 mg Fe/kg diet), with the biological lactating dam nursing the pups. At P7 all ID dams were fed IS diet. At P15 and P30, rats were weighed, blood was drawn, and tissues were harvested. Kidneys were weighed and fixed renal sections were blindly examined for radial glomerular counts (RGCs), glomerular size, cortical depth, glomeruli per cortical surface area and total glomerular planar surface area. P <0.05 was considered significant. Results At P15, ID pups were 20% smaller than IS pups, but only 8% smaller at P30. The ratio of kidney/rat weight was similar in all groups, except higher in P15 ID. At P15, hematocrit was lower in ID than IS, but not at P30. Glomerulogenesis was altered by gestational ID. Compared to P15 IS, RGCs in P15 ID were lower, mean glomerular size smaller, cortical depth shorter, glomerular density greater, and glomerular planar surface area lower. Microscopic renal morphometric parameters were normalized by P30. Conclusion Gestational ID caused newborn anemia, growth restriction, with smaller and more‐dense glomeruli. The kidneys adapted to equalize glomerular density and filtering area, in contrast to published work in adult offspring of gestation ID. Delayed cessation of nephrogenesis may hold potential clues to understanding fetal renal adaptation to tissue iron depletion. UW Department of Pediatrics and UW Graduate School, Meriter Foundation, Minnesota Viking Children's Fund Grant Funding Source : UW Department of Pediatrics and UW Graduate School, Meriter Foundation, Minnesota Viking Children's Fund