Assistant Professor Cincinnati Children's Hospital Medical Center Cincinnati, Ohio, United States
Background: While term infants complete nephrogenesis before birth, preterm infants must complete this process postnatally. Preterm birth is associated with low nephron endowment and increased risk of subsequent chronic kidney disease (CKD). Antenatal corticosteroids (ANS) are used to accelerate lung maturity in preterm neonates. In animal models, ANS have been shown to impair kidney branching and accelerate maturation of glomeruli, but the studies are limited to prenatal steroid use. Postnatal steroids are used to improve lung function but may have unintended consequences, including worse 2-year neurodevelopmental outcomes in the Preterm Erythropoietin Neuroprotection (PENUT) trial. In the PENUT cohort, 18% had an estimated glomerular filtration rate (eGFR) < 90 ml/min per 1.73 m2 at two years of age, but the association of postnatal steroid use on kidney function is unknown. Objective: To determine if duration of postnatal corticosteroids in preterm infants influences kidney function at 24 months corrected age. We hypothesized that 2-year eGFR would be decreased in those with early exposure or prolonged corticosteroid use. Design/Methods: A secondary analysis of the PENUT trial was performed evaluating the frequency and duration of postnatal steroid exposure. Infants who survived hospital discharge with blood samples at 22-26 months corrected age were included. The primary outcome was eGFR < 90 ml/min/1.73 m2 using the CKiD serum creatinine/Cystatin C equation. Adjustments were made for gestational age, sex, APGAR, size for gestational age, severe sepsis, necrotizing enterocolitis, bronchopulmonary dysplasia, intestinal perforation, intraventricular hemorrhage, retinopathy of prematurity, and respiratory support at discharge. Results: 838 surviving infants were included (Table 1). 397 (47%) were steroid-exposed. Dexamethasone was the most common exposure (n = 238, median start day of life (DOL) 27 with median duration 8 days) followed by hydrocortisone (n = 232, median start DOL 13, median duration 17 days). 348 infants were evaluated at 22–26-month follow-up, and 61 (17.5%) had blood samples (Table 2). Hydrocortisone duration of 1-7 days was associated with increased odds (aOR: 2.86, 95% CI: 1.07-7.68) of decreased eGFR (Table 3). All other steroid exposures and durations were not associated with decreased eGFR.
Conclusion(s): Overall, postnatal steroid exposure was not associated with decreased eGFR at 24 months corrected age, except for a short course of hydrocortisone. This study was limited by kidney function assessment in follow-up, and further studies are needed to assess for associations.