Abstract

Increased investment in perinatal health in developing countries has improved the survival of preterm newborns, but their significant multiorgan immaturity is associated with short and long-term adverse consequences. Cathepsin B, as a protease with angiogenic properties, may be related to the process of nephrogenesis. A total of 88 neonates (60 premature children, 28 healthy term children) were included in this prospective study. We collected urine samples on the first or second day of life. In order to determine the concentration of cathepsin B in the urine, the commercially available enzyme immunoassay was used. The urinary concentrations of cathepsin B normalized with the urinary concentrations of creatinine (cathepsin B/Cr.) in newborns born at 30–34, 35–36, and 37–41 (the control group) weeks of pregnancy were (median, Q1–Q3) 4.00 (2.82–5.12), 3.07 (1.95–3.90), and 2.51 (2.00–3.48) ng/mg Cr, respectively. Statistically significant differences were found between the group of newborns born at 30–34 weeks of pregnancy and the control group (p < 0.01), and between early and late preterm babies (PTB) (p < 0.05). The group of children born at 35–36 weeks of pregnancy and the control group did not differ significantly. This result suggests that the elevated urinary cathepsin B/Cr. level may be the result of the kidneys’ immaturity in preterm newborns.

Highlights

  • Preterm birth accounts for 11% of births worldwide [1]

  • The glomerular and tubular maturation of the kidneys of preterm newborns may be confounded by the nephropathy of prematurity and acute kidney injury (AKI), whose incidence in neonates is estimated at 8–24% of children hospitalised in the Intensive Neonatal Care Units

  • Length, and head and chest circuits were significantly lower in premature neonates than in term children; all the children were appropriate for gestational age

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Summary

Introduction

Preterm birth (before 37 completed weeks of gestation) accounts for 11% of births worldwide [1]. Nephrogenesis in humans ends by approximately 34–36 weeks of gestation, with over 60% of nephrons being formed during the last trimester [6]. In premature neonates, normal nephrogenesis is interrupted, and both nephron number and kidney size are reduced [7]. While nephrogenesis may continue in premature neonates for up to 40 days following birth, these nephrons are not normal and age at an increased rate [8]. Despite this postnatal development of the kidneys, premature children are still left with a lower number of nephrons. One-third of this group are premature babies [7,11,12,13]

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