Search

To investigate the risk factors for death in critically ill neonates receiving continuous renal replacement therapy (CRRT). This retrospective study analyzed the clinical data of critically ill neonates receiving CRRT at two tertiary hospitals from January 2015 to December 2021. A multi-factor logistic regression analysis was performed, and the predictive value of relevant risk factors on death was verified by receiver operating characteristic (ROC) curve. A total of 59 cases of critically ill neonates were included in this study, with a mortality of 37.3%. The most common primary disease in these cases was neonatal sepsis, followed by neonatal asphyxia, and inborn errors of metabolism (IEM). Univariate analysis showed that the risk factors related to death included primary diseases; the number of organs involved in multiple organ dysfunction syndrome (MODS), neonatal critical illness scores (NCIS), and indications of CRRT; the blood lactate, blood glucose, hemoglobin, and platelet before CRRT initiation; and the incidence of bleeding or thrombosis during CRRT. Multi-factor logistic regression analysis showed that risk factors for death in critically ill neonates receiving CRRT included the occurrence of neonatal sepsis, the number of organs involved in MODS, and the NCIS. ROC curve analysis showed that the number of organs involved in MODS and NCIS had a good predictive value for death in critically ill neonates receiving CRRT, with the areas under the curve (AUC) being 0.700 and 0.810, respectively.Neonatal sepsis, the number of organs involved in MODS, and NCIS were independent risk factors for death in critically ill neonates receiving CRRT. Moreover, the number of organs involved in MODS and NCIS could effectively predict death in critically ill neonates receiving CRRT.• The population to which CRRT is applicable is gradually expanding from critically ill children to critically ill neonates. • The mortality of critically ill neonates receiving CRRT remains high.• The most common primary disease in critically ill neonates receiving CRRT was neonatal sepsis, followed by neonatal asphyxia and inborn errors of metabolism (IEM). • The number of organs involved in MODS and NCIS could effectively predict death in critically ill neonates receiving CRRT.

Background Pulmonary hypertension (PH) is a common complication of bronchopulmonary dysplasia (BPD) in very-low-birth-weight infants (VLBWIs). Although recent studies have increased awareness that PH contributes significantly to the high morbidity and mortality of BPD, the risk factors and clinical characteristics for PH in VLBWIs are little known. Objectives To investigate the risk factors and clinical characteristics for BPD-associated pulmonary hypertension (BPD-PH) in VLBWIs. Methods A retrospective case–control observational study of VLBWIs with BPD admitted to a neonatal intensive care unit (NICU) over 4 years. According to echocardiograms confirming elevated pulmonary artery pressure after 28 days after birth, we divided BPD infants into PH group (n = 18) and non-PH group (n = 65). We compared pre- and postnatal characteristics between VLBWIs with or without PH. Multivariable logistic regression analysis was conducted with backward selection. Results A total of 83 infants with BPD were divided into PH group (n = 18) or non-PH group (n = 65). The average birth weight of the infants with BPD was 1078.1 g. Compared with those infants of the non-PH group, the birth weight of BPD-PH infants was significantly lower (968.1 ± 187.7 vs. 1108.5 ± 185.8, P = 0.006). Infants in the PH group had a higher incidence of patent ductus arteriosus (PDA) and underwent longer durations of oxygen therapy and mechanical ventilation compared to those in the non-PH group. In all subjects, birth weight (OR 0.995; 95% CI 0.991–0.999; P = 0.025) and PDA (OR 13.355; 95% CI 2.950–60.469; P = 0.001) were found to be specific risk factors for BPD-PH in this cohort. Conclusions The study shows PDA and birth weight are specific risk factors for BPD-PH in VLBWIs.

Objective: To investigate the risk factors for death in critically ill neonates receiving continuous renal replacement therapy (CRRT). Methods: The clinical data of critically ill neonates treated with CRRT at two tertiary hospitals from January 2015 to December 2021 were retrospectively analysed. A multi-factor logistic regression analysis was performed, and the predictive value of relevant risk factors on death was verified by receiver operating characteristic (ROC) curve. Results: (1) A total of 59 cases of critically ill neonates were included in this study, with 37 cases in the survival group and 22 in the death group. The mortality rate was 37.3%. (2) The most common primary disease in these cases was neonatal sepsis, followed by neonatal asphyxia and inborn errors of metabolism (IEM). (3) Univariate analysis showed that the risk factors related to death included primary diseases (neonatal sepsis, IEM), the number of organs involved in multiple organ dysfunction syndrome (MODS), neonatal critical illness scores (NCIS), the levels of blood lactate, blood glucose, hemoglobin, and platelet before CRRT initiation, and the incidence of bleeding or thrombosis during CRRT (all PP=0.035), the number of organs involved in MODS (OR=4.762, 95% CI 1.301 to 17.424, P= 0.018), and the NCIS (OR=0.819, 95% CI 0.715 to 0.938, P=0.004). (5) ROC curve analysis showed that the number of organs involved in MODS and NCIS had a good predictive value for death in critically ill neonates treated with CRRT, with the areas under the curve (AUC) being 0.700 and 0.810, respectively (both PConclusions: Neonatal sepsis, number of organs involved in MODS, and NCIS were independent risk factors for death in critically ill neonates treated with CRRT. Moreover, the number of organs involved in MODS and NCIS could effectively predict death in critically ill neonates treated with CRRT.

Background CRRT has attracted more and more attention in the treatment of acute neonatal hyperammonemia. Methods We retrospectively analyzed the clinical data of hyperammonemic neonates treated with CRRT in the neonatal intensive care unit (NICU) of Shanghai Children's Hospital from August 2016 to September 2021, and further explored the relationship between the rate of decrease of blood ammonia and dialysis rate. Results A total of 6 cases of neonatal hyperammonemia were included, their primary diseases were 3 cases of ornithine transcarbamyltransferase deficiency (OTCD), 1 case of carbamoyl phosphate synthetase 1 deficiency (CPS1D), 1 case of methylmalonic acidemia (MMA) with homocysteinemia (combined MMA) and 1 case of transient hyperammonemia. All infants developed impaired consciousness, convulsions and severe hyperammonemia, so CRRT was superimposed on diet control and medication, and the mode of continuous venovenous hemodiafiltration (CVVHDF) was used in all cases. The gestational age at birth was (37.98 ± 1.12) weeks, the age at onset was (1.91 ± 0.91) d, and the weight at CRRT was (3157.50 ± 605.95) g. The dialysis rate was (880–3937) ml/h/1.73m2, the decrease rate of blood ammonia was (15.79–33.33) µmol/h, and the duration of CRRT diversion was 44–110 h. The decrease rate of blood ammonia increased with the increase in dialysis rate, without an increase in the incidence of serious complications. Conclusions CRRT can alleviate the metabolic crisis of hyperammonemic neonates, and increasing the dialysis rate of CRRT can safely and more effectively reduce blood ammonia levels in critically hyperammonemic neonates.

Bronchopulmonary dysplasia (BPD) is a chronic lung disease that affects the quality of life of infants. At present, premature exposure to hyperoxia for extended periods of time is believed to affect the development of lung tissue and vascularity, resulting in BPD. The oxidative stress caused by hyperoxia exposure is an important risk factor for BPD in premature infants. Nuclear factor E2‐related factor 2 (Nrf2) is an important regulator of antioxidant mechanisms. As a microRNA, microRNA‐125b (miR‐125b) plays an important role in cell proliferation, differentiation and apoptosis. Although the Nrf2/ARE pathway has been extensively studied, little is known about the regulatory role of microRNAs in Nrf2 expression. In this study, the expression levels of Nrf2 and miR‐125b in the lung tissues of premature Sprague Dawley (SD) rats and A549 cells exposed to hyperoxia were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR), and the apoptosis of A549 cells was detected by flow cytometry. The results showed that Nrf2 and miRNA‐125b in the lung tissues of premature rats increased significantly upon exposure to hyperoxia and played a protective role. Nrf2 was suppressed by small interfering RNA (siRNA) in A549 cells, miR‐125b was similarly inhibited, and apoptosis was significantly increased. These results suggest that miR‐125b helps protect against BPD as a downstream target of Nrf2.

Background Bronchopulmonary dysplasia (BPD) is a common respiratory disease in premature infants and is characterized by alveolar and pulmonary vascular dysplasia. Long-term oxygen exposure can cause BPD in preterm infants. Numerous studies have shown that long non-coding ribonucleic acid (lncRNA) is involved in the process of biological metabolism; however, its role in the development of BPD is unclear. Apoptosis-induced factor (AIF) is a key component involved in apoptosis. The Kelch-like ECH-associated protein 1/nuclear factor erythroid-2-related factor 2 (Keap1/Nrf2) signaling pathway is a body-derived antioxidant signaling pathway. Methods In this study, the relative expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), AIF, Keap1, and Nrf2 was detected by real-time polymerase chain reaction (PCR). Also, the apoptosis of A549 cells was detected by flow cytometry. Results The results showed that, compared to the control group, the expression of MALAT1 increased significantly, and AIF decreased substantially in BPD premature infants. In the A549 hyperoxic lung injury model, compared with the air group, the expression of MALAT1 in the hyperoxia group decreased markedly, while the expression of Keap1 and Nrf2 increased considerably. Furthermore, compared with the control plasmid transfection air group (NC group), the expression of Keap1 and Nrf2 increased significantly in the small interfering RNA (siRNA) group. Conclusions These results indicate that MALAT1 can play a protective role in BPD via the reduction of apoptosis and anti-oxidation, offering clinicians a new way to prevent and treat BPD.

Bronchopulmonary dysplasia (BPD) is one of the main causes of chronic lung disease in premature infants. Acute lung injury following exposure to hyperoxia contributes to the development of BPD in preterm infants. The nuclear factor‑erythroid 2‑related factor 2 (Nrf2) signaling pathway is an endogenous antioxidant defense mechanism that is involved in the pathogenesis of numerous hyperoxia‑induced diseases. In the present study, the expression of Nrf2, Kelch‑like ECH‑associated protein 1 (Keap1) and NAD(P)H quinone oxidoreductase 1 enzyme (NQO1) was detected in A549 cells exposed to hyperoxia and transfection with small interfering RNA (siRNA) using reverse transcription‑quantitative polymerase chain reaction and western blotting, and cellular apoptosis was detected using flow cytometry. The results demonstrated that apoptosis increased significantly following exposure of the cells to hyperoxia, and Nrf2, Keap1 and NQO1 expression levels were significantly upregulated under hyperoxic conditions. Furthermore, following transfection with Nrf2 siRNA, the expression levels of these genes were significantly downregulated and apoptosis was significantly increased compared with the respective values in untransfected cells. These findings suggest that the Nrf2‑Keap1‑antioxidant response element‑NQO1 signaling pathway may play a protective role in hyperoxia‑induced lung injury via the inhibition of apoptosis.

Bronchopulmonary dysplasia (BPD) is a chronic lung disease with long-term sequelae including neurodevelopmental delay. Although the precise mechanism of BPD is not well defined, oxidative stress is thought to be involved in the pathogenesis process of BPD. Nrf2 (Nuclear factor erythroid 2-related factor 2)-Keap1 (Kelch-like ECH associated protein 1)-ARE (Antioxidant Reaction Elements) signaling pathway is one of the main protective mechanisms of BPD, which can induce cytoprotective gene expression, such as heme oxygenase‐1 (HO-1), nicotinamide quinone oxidoreductase 1 (NQO1) and so on. We exposed premature rats to hyperoxia and identified lung developmental retardation in preterm rats, with similar pathological changes as BPD. The expression of Nrf2 and HO-1 in premature rats was significantly higher after hyperoxia exposure. To explore the changes of Nrf2 and HO-1 in premature rats and enhance their beneficial functions may provide new treatment strategies for infants at risk of BPD.

Carboxy-terminated 4-arm star-shaped e-caprolactone oligomers (Tetra-SA-CLO, Tetra-PA-CLO, and Tetra-TCPA-CLO) were synthesized by the reactions of hydroxy-terminated 4-arm star-shaped e-caprolactone oligomers (Tetra-OH-CLO) having the degree of polymerization per one oligocaprolactone chain, n = 3 and 5 with succinic anhydride, phthalic anhydride, and 2,3,4,5-tetrachlorophthalic anhydride, respectively. As a pyridyl-terminated analog, nicotinate-functionalized 4-arm star-shaped e-caprolactone oligomer (Tetra-NA-CLO) was synthesized by the esterification reaction of Tetra-OH-CLO with nicotinic acid. All mixtures of the carboxy- and pyridyl-terminated analogs became thermoreversible organogels in N , N -dimethylformamide and nitromethane at around 15 °C. The 1 H NMR and FT-IR analyses of the mixtures revealed the formation of hydrogen-bonded polymer network. The glass transition and cold crystallization temperatures of the mixtures were higher than the values estimated from those of the single components.