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Urinary podocalyxin as a possible novel marker of intrauterine nephrogenesis and extrauterine podocyte injury

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Abstract

Background

The number of nephrons at birth is determined during fetal development and is modulated thereafter by postnatal podocyte injury. Hyperfiltration, caused by a reduced number of nephrons, is a risk factor for chronic kidney disease. It is therefore important to monitor the formation of nephrons.

Methods

Urine samples were collected from infants within 1–2 days of birth, with follow-up sampling for preterm infants at 37–39 weeks of corrected age. Urinary levels of podocalyxin (PCX), β2-microglobulin (β2MG), N-acetyl-ß-D-glucosaminidase (NAG), total protein (TP), microalbumin (mAlb) and creatinine were measured and the relationship between these markers evaluated.

Results

Seventy-nine neonates were enrolled in this study. Urinary levels of PCX at birth were higher than normal adult reference values, with levels increasing up to a gestational age of 36 weeks (p = 0.0242). At 37–39 weeks corrected age, urinary levels of PCX decreased to adult levels. The levels of PCX in the urine at birth were not correlated to urinary levels of β2MG, NAG, TP and mAlb.

Conclusions

An increased urinary level of PCX may be a marker of both active nephron formation and podocyte injury sustained at birth. As such, changes in urinary levels of PCX are likely to reflect adaptation of renal function to the extra-uterine environment.

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Correspondence to Taihei Hayashi.

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The study was approved by the Institutional Ethics Committee at the University of Fukui (# 20140014). Informed consent was obtained from the parents.

Conflict of interest

All authors declare that they do not have any relevant conflict of interests regarding this paper.

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Hayashi, T., Tokuriki, S., Okuno, T. et al. Urinary podocalyxin as a possible novel marker of intrauterine nephrogenesis and extrauterine podocyte injury. Pediatr Nephrol 32, 1891–1896 (2017). https://doi.org/10.1007/s00467-017-3676-6

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  • DOI: https://doi.org/10.1007/s00467-017-3676-6

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