A congenital or programmed reduction in glomerular number increases the susceptibility to hypertension and kidney injury in adulthood thus, premature birth or low birth weight, leading to a low glomerular endowment, can be associated with these two diseases. Renal morphogenesis is sensitive to hypoxia which is a physiological trigger for the expression of vascular endothelial growth factor. On the other hand, hyperoxia increases oxidative stress and adversely affects glomerular and tubular development, and is associated with a substantial reduction of renal klotho expression in adulthood. Preterm newborns are often submitted to oxygen therapy, exposing them to an acute high-oxygen level situation, in contrast to the intrauterine low-oxygen environment. Investigating the role of klotho on kidney development leads to the understanding of the possible mechanisms related to disorders in the preterm neonatal kidney exposed to hyperoxia and its long term effects in adulthood.
Keywords: Angiogenesis; VEGF; hyperoxia; postnatal nephrogenesis.