Abstract
Neonatal acute kidney injury (nAKI) is highly prevalent but the definition of nAKI remains nebulous. This is because we rely on serum creatinine (SCr) for the estimation of kidney function which is an indirect measure of muscle mass and the maternal placental transfer of SCr in the early post-natal period. Similarly, the physiological transition into the extra-uterine environment should result in a natural improvement in neonatal renal function from 25% to at least 60% of adult renal function within the first post-natal week. This should lead to a natural and steady decline in the SCr from birth to discharge. Neonatal AKI may be defined as a rise in SCr of >0.3 mg/dL, a peak in SCr ≥1.5 mg/dL and/or a “nadir” SCr at discharge ≥0.5 mg/dL. Importantly, infants born preterm and/or small for gestational age are more vulnerable to nAKI. Diagnosis, early medical intervention and longterm follow-up are essential for these individuals to avert the likely progression to chronic kidney disease including hypertension and cardiorenal disease with shortened longevity.