Prematurity disrupts glomeruli development, whereas prematurity and hyperglycemia lead to altered nephron maturation and increased oxidative stress in newborn baboons.
Prematurity disrupts glomeruli development, whereas prematurity and hyperglycemia lead to altered nephron maturation and increased oxidative stress in newborn baboons.
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DOI：
10.1038/pr.2017.290
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发表时间：
2018-03
影响因子：
3.6
通讯作者：
Blanco CL
中科院分区：
文献类型：
--
作者：
Callaway DA;McGill-Vargas LL;Quinn A;Jordan JL;Winter LA;Anzueto D;Dick EJ Jr;Blanco CL
Premature birth occurs when nephrogenesis is incomplete and has been linked to increased renal pathologies in the adult. Metabolic factors complicating preterm birth may have additional consequences for kidney development. Here, we evaluated the effects of prematurity and hyperglycemia on nephrogenesis in premature baboons when compared to term animals. Baboons were delivered prematurely (67% gestation; n=9) or at term (n=7) and survived 2–4 weeks. Preterm animals were classified by glucose control during the first five days of life (DOL): normoglycemic (PtN; serum glucose 50–100mg/dL, n=6) and hyperglycemic (PtH; serum glucose 150–250mg/dL, n=3). Kidneys were assessed histologically for glomeruli relative area, maturity, size, and overall morphology. Kidney lysates were evaluated for oxidative damage with 4-hydroxynonenal (4-HNE) antibody. Histological examination revealed decreased glomeruli relative area (p<0.05), fewer glomerular generations (p<0.01), and increased renal corpuscle area (p<0.001) in preterm compared to term animals. Numbers of apoptotic glomeruli were similar between groups. PtH kidneys exhibited reduced nephrogenic zone width (p<0.0001), increased numbers of mature glomeruli (p<0.05), and increased 4-HNE staining compared to PtN kidneys. Prematurity interrupts normal kidney development, independent of glomerular cell apoptosis. When prematurity is complicated by hyperglycemia; kidney development shifts towards accelerated maturation and increased oxidative stress.
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