Abstract
Preterm neonates are prematurely exposed to high oxygen levels at birth which may adversely impact ongoing renal development. The aim of this study was to determine the effects of neonatal hyperoxia exposure on renal function and morphology with aging. Sprague Dawley rat pups were raised in a hyperoxic environment (80% oxygen) from P3 to P10 during ongoing postnatal nephrogenesis. Control litters were kept in room air (n = 6–8 litters/group; one male, one female/litter/age). Kidney function (urine and plasma creatinine, sodium, and protein) and morphology (renal corpuscle size, glomerulosclerosis, fibrosis, and glomerular crescents) were assessed at 1, 5, and 11 months of age. Neonatal hyperoxia exposure had no impact on body or kidney weights. Creatinine clearance was significantly reduced following hyperoxia exposure at 5 months; there was no significant effect on renal function at 1 or 11 months. The percentage of crescentic glomeruli (indicative of glomerular injury) was markedly increased in 11 month hyperoxia‐exposed males. Renal corpuscle size, glomerulosclerosis index, and renal fibrosis were not affected. Findings suggest that exposure to high oxygen levels during development may impact renal functional capacity and increase susceptibility to renal disease in adulthood depending on age and sex.
Highlights
We have previously shown in a rodent model of neonatal hyperoxia exposure (80% O2 from postnatal days [P] 3 to 10, encompassing a period of active postnatal nephrogenesis in the rat) that there are indications of impaired renal development, with pups exhibiting a significantly reduced nephrogenic zone and glomerular size at P5 (Popescu et al 2013)
The pups of the dam used for interchange served as a control for the effects of the dam being exposed to hyperoxia, but the pups themselves were maintained in room air (Popescu et al 2013)
We have shown that exposure to hyperoxia in the neonatal period results in alterations in renal function and pathology in aging rats
Summary
There is emerging evidence linking preterm birth (birth prior to 37 completed weeks of gestation) with impaired renal development (Rodriguez et al 2004; Sutherland et al 2011), reduced kidney size (Keijzer-Veen et al 2010; Zaffanello et al 2010; Kwinta et al 2011), renal dysfunction (Rodriguez-Soriano et al 2005; Iacobelli et al 2007), hypertension (Dalziel et al 2007; Cooper et al 2009; de Jong et al 2012), and renal disease (Hodgin et al 2009; Ikezumi et al 2013). Long-Term Renal Impact of Neonatal Hyperoxia preterm neonates (Gubhaju et al 2011; Sutherland et al 2014) This may occur through either exposure to room air or mechanical ventilation (up to 100% supplemental oxygen, Tan et al 2005; Rabi et al 2011); blood oxygen concentrations rise immediately after birth (Kamlin et al 2006; Rabi et al 2006) compared to in utero which is an optimal (low oxygen: Rodesch et al 1992; Fischer and Bavister 1993) environment for fetal kidney development (Tufro-McReddie et al 1997). Oxidative stress is implicated in a number of diseases of prematurity, such as bronchopulmonary dysplasia and retinopathy, which are characterized by impaired angiogenesis, apoptosis, and inflammation (Smith 2003; Thebaud and Abman 2007; Saugstad et al 2012)
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