Abstract
Acute kidney injury (AKI) in neonates presents a unique and ongoing challenge in the early diagnosis and subsequent management of these most vulnerable patients. The globally accepted traditional renal functional marker, serum creatinine (SCr), has long been recognized as unreliable in the neonate, particularly in those born preterm and of low birth weight [1]. In the immediate post-natal week, physiologic adjustments in systemic and renal perfusion lead to an increase in glomerular filtration rate (GFR) from as low as 20 ml/min/1.73 m2 to as high as 60 ml/min/1.73 m2 in term infants [1, 2]. Full maturation of GFR will not be achieved until about 2 years of age. Accordingly, the SCr is initially elevated due to the burden of excreting maternal creatinine. This accounts for a pattern of the SCr rising shortly after birth with a subsequent fall to a nadir <0.4 mg/dL (35 μM/L) in infants with normal post-natal renal development. In contrast, infants born preterm are more likely to have a decreased number of nephrons relative to their shortened gestation as well as intrauterine and perinatal stressors which impede a smooth and positive improvement in GFR [1, 2]. Hence, SCr may be inordinately elevated with a delay in decline to an appropriate nadir. A “true” measure of GFR or recognition of any degree of early kidney injury has been elusive in this setting [2]. While continuing to refine SCr-based definitions of neonatal AKI, a few pioneers have focused research efforts in the emerging field of “omics” in systems biology [3–5]. The suffix, “omics” emerged at the turn of the century to designate a field of biology devoted to the use of high throughput technologies to characterize the molecules that define the structure and function of an organism [5, 6]. Hence, the terms “genomics,” “proteomics,” “metabolomics” and others can be applied to better understand the pathophysiology and to develop biomarkers for the early diagnosis and treatment of neonatal AKI (Fig. 16.1).