MR SUTHERLAND1, D RYAN1, B DAVISON2, M CHATFIELD2, S DIWAKARLA3, WE HOY4, G SINGH2,5, MJ BLACK1
1Monash University, Clayton, VIC; 2Menzies School of Health Research, Charles Darwin University, Darwin, NT; 3Florey Institute of Neuroscience and Mental Health, Parkville, VIC; 4University of Queensland, Brisbane, QLD; 5Royal Darwin Hospital, Darwin, NT.
Aim: To examine the impact of preterm birth (delivery prior to 37 completed weeks of gestation) on early postnatal renal function in Indigenous and non-Indigenous neonates.
Background: The incidence of renal disease in Australia is disproportionately high amongst Indigenous populations. The cause of renal disease is multifactorial, but impaired renal development in early life is likely an important antecedent. Preterm birth (affecting ~8% of all Australian infants, and ~14% of Indigenous infants) can occur when nephrogenesis is still ongoing; renal function in preterm neonates may be adversely affected by renal immaturity and/or injury.
Methods: Indigenous (n=60) and non-Indigenous (n=42) infants were grouped by gestational age at birth: < 28, 29–32, and 33-36 weeks. Twenty-four hour pooled urine samples were obtained on days 3-7, 14, 21 and 28 to assess creatinine clearance (CrCl), and the fractional excretion of sodium (FeNa). Spot urine samples taken weekly were assessed for urine total protein, albumin, and beta-2 microglobulin levels.
Results: Compared to non-Indigenous neonates, Indigenous neonates exhibited significantly increased beta-2 microglobulin excretion on days 8 and 15, and Indigenous neonates born extremely preterm (≤ 28 weeks gestation) also had significantly increased FeNa levels over the first month of life; these findings are indicative of impaired tubular function. Pathological proteinuria (urine total protein > 500 mg/L) was evident in 13% of Indigenous preterm infants compared to 4% of non-Indigenous preterm infants.
Conclusions: These findings demonstrate that early neonatal renal dysfunction following preterm birth is exacerbated in Indigenous infants, and this may be reflective of impaired intrauterine renal development and/or a greater vulnerability to postnatal renal injury.