Factors associated with survival in paediatric and adolescent renal cell carcinoma: a population-based study.

BACKGROUND: The purpose of this study was to conduct a population-based study to determine the prognosis of renal cell carcinoma (RCC) in children and adolescents. METHODS: Patients with RCC who were registered in the Surveillance, Epidemiology, and End Results (SEER) program between 2000 and 2018 had their demographic and clinical characteristics evaluated retrospectively. The log-rank test was used to compare survival curves. Kaplan-Meier estimates were used to generate survival curves based on various factors. To identify factors associated with overall survival, Cox proportional-hazards regression was used. RESULTS: A total of 251 patients were enrolled in the study. For all patients, the overall survival (OS) rates at 3- and 5- year were 93.5% and 92.0%, respectively. A multivariable study revealed that the following factors were independently associated with overall survival: sex, race, histologic type, SEER stage, AJCC stage, and type of surgery. Cox analysis showed that white patients had the lowest risk of mortality (hazard ratio (HR) 2.58, 95% confidence interval (CI), 1.33-4.99; P = 0.005), compared with black patients. Patients having metastatic disease had significantly higher mortality risk (HR 43, 95% CI, 14.8-125; P < 0.001) than the patients with localized tumour. CONCLUSIONS: Our study emphasizes the importance of race, SEER stage, and surgery in the prognosis of paediatric RCC, providing valuable epidemiological evidence for clinical practice. Economic studies assessing a race/ethnic group specific strategy are also required.

Single-incision versus conventional laparoscopic pyloromyotomy for pediatric hypertrophic pyloric stenosis: a systematic review and meta-analysis.

PURPOSE: To assess the safety and efficacy of single-incision versus conventional laparoscopic pyloromyotomy in pediatrics, we conducted a systematic review and meta-analysis. METHODS: A literature search was conducted to identify studies that compared single-incision laparoscopic pyloromyotomy (SILP) and conventional laparoscopic pyloromyotomy (CLP) for infants with hypertrophic pyloric stenosis (HPS). Meta-analysis was used to pool and compare variables such as operative time, time to full feeding, length of hospital stay, mucosal perforation, inadequate pyloromyotomy, wound infection, incisional hernia and overall complications. RESULTS: Among the 490 infants with HPS in the seven studies, 205 received SILP and 285 received CLP. There was significant longer time to full feeding for SILP compared with CLP. However, pooling the results for SILP and CLP revealed no significant difference in operative time, length of hospital stay and postoperative complications. CONCLUSIONS: SILP is a safe, feasible and effective surgical procedure for infants with HPS when compared to CLP. SILP is equivalent to CLP in terms of operative time, length of hospital stay and postoperative complications. We conclude that LS should be considered an acceptable option for HPS.

Glutathione metabolism rewiring protects renal tubule cells against cisplatin-induced apoptosis and ferroptosis.

Renal proximal tubular cells are highly vulnerable to different types of assaults during filtration and reabsorption, leading to acute renal dysfunction and eventual chronic kidney diseases (CKD). The chemotherapeutic drug cisplatin elicits cytotoxicity causing renal tubular cell death, but its executing mechanisms of action are versatile and elusive. Here, we show that cisplatin induces renal tubular cell apoptosis and ferroptosis by disrupting glutathione (GSH) metabolism. Upon cisplatin treatment, GSH metabolism is impaired leading to GSH depletion as well as the execution of mitochondria-mediated apoptosis and lipid oxidation-related ferroptosis through activating IL6/JAK/STAT3 signaling. Inhibition of JAK/STAT3 signaling reversed cell apoptosis and ferroptosis in response to cisplatin induction. Using a cisplatin-induced acute kidney injury (CAKI) mouse model, we found that inhibition of JAK/STAT3 significantly mitigates cisplatin nephrotoxicity with a reduced level of serum BUN and creatinine as well as proximal tubular distortion. In addition, the GSH booster baicalein also reclaims cisplatin-induced renal tubular cell apoptosis and ferroptosis as well as the in vivo nephrotoxicity. In conclusion, cisplatin disrupts glutathione metabolism, leading to renal tubular cell apoptosis and ferroptosis. Rewiring glutathione metabolism represents a promising strategy for combating cisplatin nephrotoxicity.