Acute kidney Injury (AKI) prior to the completion of nephrogenesis at 34 weeks’ gestation has significant life-long effects. The immature kidney only receives 3-4% of total cardiac output, compared to 20% in term infants, children and adults. Therefore, minimal decreases in oxygen delivery may substantially compromise proper oxygen utilization increasing the risk for morphologic changes and reduced nephron endowment. Current diagnostic criteria (serum creatinine (sCr) elevations with oliguria) cannot detect early-onset AKI, as up to 50% of nephron damage has already occurred by the time these abnormalities become apparent. This presentation will look at new research related to the current diagnostic criteria for AKI in the preterm infant, the physiologic mechanisms involved in AKI and short and long-term implications.
Learning Objectives:
1. Describe current diagnostic criteria for Acute Kidney Injury (AKI) in the preterm and term infant.
2. Identify the physiologic mechanisms involved in renal oxygenation measurement using near-infrared spectroscopy technology.
3. Describe the short and long-term implications associated with AKI development in the preterm population.
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