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Am J Perinatol. 2012 Feb;29(2):115-20. doi: 10.1055/s-0031-1295651. Epub 2011 Nov 17.

Oligonephropathy of prematurity.

Author information

1
Department of Neonatology, The Townsville Hospital, Douglas, Queensland, Australia. Yoga_Kandasamy@health.qld.gov.au

Abstract

With improved health care, the number of premature babies who survive to adulthood is expected to increase. The objective of this review is to determine whether premature infants have an increased risk of chronic kidney disease (CKD). A literature review was performed by searching PubMed (U.S. National Library of Medicine) and the Cochrane Library, using the keywords "prematurity," "kidney," "nephrogenesis," "oligonephropathy," and "kidney impairment." Articles published in English since 1990 were reviewed. Increasing evidence suggests that prematurity causes oligonephropathy independently of, and coexisting with, intrauterine growth restriction. Animal studies show that nephrogenesis continues for up to 3 weeks in extrauterine life, but with up to 18% abnormal glomeruli. Nephrogenesis is further impaired in preterm infants who develop renal impairment in the early postnatal period, which is estimated to be 8 to 24%. Premature infants are at risk for CKD. A larger longitudinal study is needed that follows up premature infants to determine the exact incidence of CKD. Until then, renal assessment in premature infants should be incorporated into follow-up guidelines, in addition to the current assessment of growth and neurodevelopmental outcomes. The cost implications to a comprehensive program, impact of early identification, and strategies to improve outcomes in this population are needed.

PMID:
22094915
DOI:
10.1055/s-0031-1295651
[Indexed for MEDLINE]

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