AKI occurred in 40% of very low birth weight infants and was concentrated in the most premature and severely ill infants. One in six infants experienced multiple episodes of AKI, and a small number of infants was discharged with an elevated serum creatinine. Reporting a history of AKI in the discharge summary occurred infrequently, and referral to a nephrologist for AKI follow-up did not occur, highlighting areas for quality improvement.

VLBW infants are frequently exposed to nephrotoxic medications, receiving approximately two weeks of nephrotoxic medications before discharge or 1 for every 6 d of hospitalization. The greatest exposure occurred among the smallest, most immature infants and those who experienced AKI.

Acute kidney injury I Pediatric I Continuous renal replacement therapy I Biomarker I Renal angina Opinion statement The term acute kidney injury (AKI) has replaced the outdated term acute renal failure throughout the literature and clinical practice. The term Binjury^highlights the spectrum of organ injury that may occur and reflects the fact that even small changes in serum creatinine (rise of 0.3 mg/dL) can be associated with adverse outcomes. A major advance in the field of AKI research has been the development of standardized staged definitions of AKI that allow for comparison of incidence, prevalence, and outcomes across studies. The Kidney Disease: Improving Global Outcomes (KDIGO) AKI definition represents the most recent consensus definition which is currently recommended for use in pediatric populations. Utilization of standard AKI definitions has made it clear that AKI occurs often in hospitalized patients and is associated with adverse short-term and long-term outcomes (hospital length of stay, mortality, subsequent chronic kidney disease). Awareness of the impact of AKI has resulted in increased efforts to understand, diagnose, prevent, and manage AKI earlier in the course of illness. While attempts at finding a treatment for AKI have been unsuccessful, largely due to the lack of sensitivity of the primary biomarker, serum creatinine, there have been many major advances in this field over the last 15 years. The development of novel biomarkers to predict the development of AKI in a timely manner and improve diagnostic accuracy is being pioneered by pediatric AKI researchers. The development of risk stratification scores (renal angina) and functional bedside tests (furosemide stress test) is enhancing our use of these biomarkers and our ability to predict those patients most likely to develop severe AKI. The recognition of the impact of fluid overload on mortality and hospital length of stay in patients with severe AKI has prompted more timely and frequent use of renal replacement therapy in critically ill children. Finally, we are recognizing that children who suffer AKI are at long-term risk for the development of chronic kidney disease and warrant follow-up.

Elevated serum uric acid is associated with hypertension and chronic kidney disease. We evaluated the relationship between birthweight and uric acid in a nationally representative sample of 5390 US adolescents aged 12-15 in the National Health and Nutrition Examination Survey from 1999 to 2012. There was an inverse association between birthweight and uric acid after adjustment for sex, age, race, obesity, and dietary sodium intake. Each 1 kg increase in birthweight was associated with decreased uric acid by 0.11 mg/dL (95% CI: -0.16 to -0.06; model R = 0.32). This relationship was stronger in adolescents with elevated blood pressure (β = -0.25; 95% CI: -0.44 to -0.06; R = 0.50) but persisted in adolescents with normal blood pressure (β = -0.10; 95% CI: -0.15 to -0.05; R = 0.31). In conclusion, lower birthweight is associated with higher uric acid in US adolescents. These findings may support the hypothesis that reduced nephron number is associated with elevated uric acid.

Calcineurin inhibitors are highly efficacious immunosuppressive agents used in pediatric kidney transplantation. However, calcineurin inhibitor nephrotoxicity (CNIT) has been associated with the development of chronic renal allograft dysfunction and decreased graft survival. This study evaluated 37 formalin-fixed paraffin-embedded biopsies from pediatric kidney transplant recipients using gene expression profiling. Normal allograft samples (n = 12) served as negative controls and were compared to biopsies exhibiting CNIT (n = 11). The remaining samples served as positive controls to validate CNIT marker specificity and were characterized by other common causes of graft failure such as acute rejection (n = 7) and interstitial fibrosis/tubular atrophy (n = 7). MiRNA profiles served as the platform for data integration. Oxidative phosphorylation and mitochondrial dysfunction were the top molecular pathways associated with overexpressed genes in CNIT samples. Decreased ATP synthesis was identified as a significant biological function in CNIT, while key toxicology pathways included NRF2-mediated oxidative stress response and increased permeability transition of mitochondria. An integrative analysis demonstrated a panel of 13 significant miRNAs and their 33 CNIT-specific gene targets involved with mitochondrial activity and function. We also identified a candidate panel of miRNAs/genes, which may serve as future molecular markers for CNIT diagnosis as well as potential therapeutic targets.