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Review
. 2024 Jul;39(7):2001-2013.
doi: 10.1007/s00467-023-06208-1. Epub 2023 Nov 10.

From premature birth to premature kidney disease: does accelerated aging play a role?

Keia R Sanderson  1 , Christel Wekon-Kemeni  2   3 , Jennifer R Charlton  4
Affiliations
Review

From premature birth to premature kidney disease: does accelerated aging play a role?

Keia R Sanderson et al. Pediatr Nephrol. 2024 Jul.

Abstract

As the limits of fetal viability have increased over the past 30 years, there has been a growing body of evidence supporting the idea that chronic disease should be taken into greater consideration in addition to survival after preterm birth. Accumulating evidence also suggests there is early onset of biologic aging after preterm birth. Similarly, chronic kidney disease (CKD) is also associated with a phenotype of advanced biologic age which exceeds chronologic age. Yet, significant knowledge gaps remain regarding the link between premature biologic age after preterm birth and kidney disease. This review summarizes the four broad pillars of aging, the evidence of premature aging following preterm birth, and in the setting of CKD. The aim is to provide additional plausible biologic mechanisms to explore the link between preterm birth and CKD. There is a need for more research to further elucidate the biologic mechanisms of the premature aging paradigm and kidney disease after preterm birth. Given the emerging research on therapies for premature aging, this paradigm could create pathways for prevention of advanced CKD.

Keywords: Acute kidney injury; Chronic kidney disease; ELGANS; Infants; Neonates; Premature aging; Very low birth weight.

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Conflict of interest statement

Declarations

Conflict of interest The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Pathways of premature aging after preterm birth associated with chronic kidney disease (CKD) and potential non-pharmacologic and pharmacologic interventions. Created with BioRender.com
Fig. 2
Fig. 2
Extrapolated figure hypothesizing the cellular integrity (i.e., telomere length, cellular replication potential) and glomerular filtration rate (GFR) for persons born at term and preterm birth which is worsened by adverse early life exposures (A); and the hypothesized potential to improve molecular integrity and GFR in persons born preterm with early therapeutic interventions to reduce premature aging (B). RAASi, renin, angiotensin, aldosterone inhibitors; SGLT2, sodium glucose cotransporter-2
See this image and copyright information in PMC

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