Acute kidney injury (AKI) is associated with long-term consequences and poor outcomes in the neonatal intensive care unit. Its precocious diagnosis represents one of the hardest challenges in clinical practice due to the lack of sensitive and specific biomarkers. Currently, neonatal AKI is defined with urinary markers and serum creatinine (sCr), with limitations in early detection and individual treatment. Biomarkers and risk factor scores were studied to predict neonatal AKI, to early identify the stage of injury and not the damage and to anticipate late increases in sCr levels, which occurred when the renal function already began to decline. Sepsis is the leading cause of AKI, and sepsis-related AKI is one of the main causes of high mortality. Moreover, preterm neonates, as well as patients with post-neonatal asphyxia or after cardiac surgery, are at a high risk for AKI. Critical patients are frequently exposed to nephrotoxic medications, representing a potentially preventable cause of AKI. This review highlights the definition of neonatal AKI, its diagnosis and new biomarkers available in clinical practice and in the near future. We analyze the risk factors involving patients with AKI, their outcomes and the risk for the transition from acute damage to chronic kidney disease.

Background: International guidelines do not support the routine use of nebulized epinephrine for acute viral bronchiolitis. Despite its vasoconstrictive and bronchodilator properties, evidence remains inconclusive. Objectives: Day-6 fraction of inspired oxygen (FiO₂) adjusted for baseline FiO₂ was designated as the principal outcome; however, this outcome hierarchy was not prospectively prespecified. The analysis compared day-6 FiO₂, adjusted for baseline FiO₂, between nebulized racemic epinephrine and placebo; peripheral capillary oxygen saturation (SpO₂), respiratory rate (RR), and heart rate (HR) were secondary outcomes. Methods: This randomized, single-blind, placebo-controlled trial included 26 infants aged 0–12 months with moderate-to-severe bronchiolitis requiring respiratory support. Participants were allocated 1:1 to nebulized racemic epinephrine (group A, n = 13) or isotonic saline placebo (group B, n = 13). Outcomes were measured at baseline (T0), day 3 (T1), and day 6 (T2). The primary analysis used ANCOVA to compare T2 FiO₂ while adjusting for T0 FiO₂; mixed repeated-measures ANOVA assessed longitudinal trajectories. Results: The adjusted T2 FiO₂ difference between groups was −0.43 percentage points (95% CI −3.43 to 2.57; p = 0.772). Adjusted T2 differences were also non-significant for SpO₂ (p = 0.058), RR (p = 0.093), and HR (p = 0.487). FiO₂ decreased over time (p = 1.99 × 10⁻⁴), but the group-by-time interaction was not significant (p = 0.108); no interaction was observed for SpO₂, RR, or HR (p = 0.296, p = 0.187, and p = 0.352, respectively). Conclusions: Nebulized racemic epinephrine did not improve the trajectories of oxygen requirement, SpO₂, RR, or HR compared with placebo; improvements over time were observed in both groups.