23 For example, in infants ≤29 weeks’ GA, a rise in the SCr level of 0.6 mg/dL confers the highest prediction of mortality, whereas in infants >29 weeks’ GA, a rise of 0.3 mg/dL is of highest mortality prediction. 22, 23 In this study, the authors proposed different cutoffs for the first postnatal week by GA, compared with the subsequent weeks, and provided cutoffs by GA group. Two recent publications, including an analysis of the AWAKEN study, suggest an alternative definition for neonatal AKI. Given the interest and focus on AKI diagnostic thresholds, it is likely that a refined definition of neonatal AKI will emerge. This is further complicated when nephrotoxic medications, such as gentamicin and other aminoglycosides, are commonly prescribed to critically ill neonates and result in tubular injury. Finally, neonatal kidneys appear to be particularly susceptible to ischemic injury to the renal tubules, even after a mild and short-term insult. 13 Poor urinary concentrating ability, particularly in neonates with high insensible losses or critical illness, predisposes neonates to volume depletion and subsequent prerenal azotemia. Third, urinary concentrating ability is low at birth and reaches adult levels by 1 year of age. 12 In neonates with a physiologically low GFR, additional stressors, such as sepsis, hypoxia, hypotension, or other clinical conditions common in prematurity, may increase the risk AKI. For example, premature infants born at 26 weeks have a GFR as low as 0.7 mL/minute per kg on day 1 of age, which improves only slightly during the first several weeks of life. 12 The GFR is low in infants, both in absolute value and when corrected for body surface area (milliliters per minute per 1.73 meters 2). Second, congruent with the increased blood flow, the glomerular filtration rate (GFR) increases dramatically after birth and reaches adult levels by 2 years of age. 11 This change in blood flow can be altered by medications (such as indomethacin), perinatal asphyxia, and maternal hemorrhage, which all predispose neonates to AKI. After birth, the distribution of blood flow transitions from deeper, more mature glomeruli to superficial, cortical glomeruli. 10 Much of this increased blood flow occurs after birth, with renal blood flow doubling in the first 2 postnatal weeks. The proportion of cardiac output delivered to the kidneys increases from 5% during fetal life to 20% by 2 years. First, both renal blood flow and perfusion pressure increase over the first weeks of life in neonates. There are several core principles of neonatal physiology that uniquely impact the diagnosis and management of neonatal AKI. Future research needs to be focused on determining the optimal follow-up strategy for neonates with a history of AKI to detect chronic kidney disease. Moving forward, biomarkers, such as urinary neutrophil gelatinase–associated lipocalin, and other new technologies, such as monitoring of renal tissue oxygenation and nephron counting, will likely play an increased role in identification of AKI and those most vulnerable for chronic kidney disease. With specific continuous renal replacement therapy machines designed for neonates, this therapy is now available and is being used with increasing frequency in NICUs. New technology has resulted in advancement in prevention and improvements in the current management in neonates with severe AKI. New evidence highlights the importance of the kidney in “crosstalk” between other organs and how AKI likely plays a critical role in other organ development and injury, such as intraventricular hemorrhage and lung disease. Specific progress has been made in identifying potential preventive strategies for AKI, such as the use of caffeine in premature neonates, theophylline in neonates with hypoxic-ischemic encephalopathy, and nephrotoxic medication monitoring programs. The natural course of neonatal AKI, along with the risk factors, mitigation strategies, and the role of AKI on short- and long-term outcomes, is becoming clearer. Large multicenter studies reveal that neonatal AKI is common and independently associated with increased morbidity and mortality. In this state-of-the-art review, we highlight the major advances over the last 5 years in neonatal acute kidney injury (AKI).
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