The objective of this study was to analyze hematologic disorders, coagulation disorders, and transfusion requirements in children with continuous renal replacement therapies (CRRT). This is a retrospective analysis of a prospectively collected database of children receiving CRRT between 2010 and 2015. Patient characteristics, CRRT parameters, hematologic and coagulation parameters, and need for transfusions were recorded and analyzed. We compared patients after heart surgery and noncardiac patients, those requiring extracorporeal membrane oxygenation (ECMO) and those without ECMO, and patients with different anticoagulation therapies: heparin and citrate. Eighty-seven patients were included (69% after heart surgery). Thirty-four percentage of patients required ECMO. Hematologic alterations throughout the therapy included a descent in hematocrit from 33.6% to 30.3% (p = 0.002) and in platelet count from 159.291 to 101.163 (p < 0.001). Coagulation parameters improved as international normalized ratio decreased from 1.5 to 1.2 (p < 0.001), fibrinogen increased from 328 to 437 mg/dl (p = 0.04), and activated partial thromboplastin time (APTT) was normalized. There were no significant differences in hematologic parameters or need for blood products between patients after heart surgery and the rest of patients, or between patients receiving heparin or citrate for anticoagulation. Ninety percentage of patients received blood products, but patients on ECMO and those who deceased required more transfusions than the rest of the patients (p < 0.01). We conclude that children undergoing CRRT show a descent in hematocrit and platelet count and require large amounts of blood products, especially those ECMO and patients who died.

Background: Respiratory viral infections (RVIs) are frequent in preterm infants and may have long-term impact on respiratory morbidity, especially those with bronchopulmonary dysplasia (BDP). The immune response and respiratory are key defence elements, so the purpose of this study is to evaluate the immune response regulation and the respiratory epithelial barrier integrity in the preterm infants suffering RVIs during Neonatal Intensive Care Unit (NICU) admission. Materials and methods: Nasopharyngeal aspirate (NPA) was obtained, separating cells from supernatants. Viral detection was performed by RT-nested PCR, and gene expression by qPCR. Proteins were detected by western blot and ELISA or Luminex. Small airway epithelial cells (SAEC) were stimulated with Poly:IC and/or wounds. Results: Pre-infection samples from 26 preterm infants that later developed RVIs had less frequency of filaggrin gene expression and fewer protein levels compared to 23 noninfected controls. Conversely, filaggrin, IL-1β, MIP-1β, VEGF and HIF-1α levels were higher in pre-infection supernatant samples, being infection-risk biomarkers. IL-17A, RANTES, VEGF, and HIF-1α levels were higher during and post infection, while MCP-1 and amphiregulin were reduced after infection. Small airway epithelial cells (SAEC) stimulated by poly:IC reduced filaggrin gene expression and increased its levels at supernatant. Finally, poly:IC stimulation over SAEC increased TLR3 and TSLP expression, while reduced AREG. Conclusion: Filaggrin gene expression and protein quantity was reduced at cellular level of the NPA, while its secreted levels were increased in basal samples from infected newborns and in SAEC stimulated with poly:IC. Our findings highlight the importance of filaggrin as a factor facilitating RVIs.

Respiratory viral infections (RVIs) are frequent in preterm infants possibly inducing long-term impact on respiratory morbidity. Immune response and respiratory barriers are key defense elements against viral insults in premature infants admitted to Neonatal Intensive Care Units (NICUs). Our main goals were to describe the local immune response in respiratory secretions of preterm infants with RVIs during NICU admission and to evaluate the expression and synthesis of lung barrier regulators, both in respiratory samples and in vitro models. Samples from preterm infants that went on to develop RVIs had lower filaggrin gene and protein levels at a cellular level were compared to never-infected neonates (controls). Filaggrin, MIP-1α/CCL3 and MCP-1 levels were higher in pre-infection supernatants compared to controls. Filaggrin, HIF-1α, VEGF, RANTES/CCL5, IL-17A, IL-1β, MIP-1α and MIP-1β/CCL5 levels were higher during and after infection. ROC curve and logistic regression analysis shows that these molecules could be used as infection risk biomarkers. Small airway epithelial cells stimulated by poly:IC presented reduced filaggrin gene expression and increased levels in supernatant. We conclude that filaggrin gene and protein dysregulation is a risk factor of RVI in newborns admitted at the NICU.