Vittoria Frattolillo

Pediatric obesity represents a growing global health challenge, closely associated with increased cardiometabolic risk and long-term adverse outcomes. Although lifestyle modifications remain the cornerstone of treatment, sustained success is often limited. Emerging evidence suggests that the gut microbiota (GM) plays a pivotal role in the pathogenesis of obesity, influencing host metabolism, energy homeostasis, and systemic inflammation. This narrative review aims to provide a comprehensive and up-to-date overview of the complex interplay between GM and pediatric obesity, with a particular emphasis on microbiota-targeted interventions. These include probiotics, prebiotics, synbiotics, postbiotics, dietary modulation, and fecal microbiota transplantation (FMT). Findings from preclinical studies and early-phase clinical trials indicate that gut dysbiosis may contribute to obesity-related mechanisms, such as altered nutrient absorption, increased adiposity, and dysregulated appetite control. Interventions targeting the microbiota have shown promise in modulating inflammatory pathways and improving metabolic profiles. While preliminary findings underscore the potential of the GM as a novel adjunctive target in managing pediatric obesity, current evidence remains heterogeneous, and robust clinical pediatric data are limited. Further research is needed to clarify the therapeutic efficacy, safety, and long-term outcomes of microbiota-modulating strategies in children with obesity.

Background/Objectives: Unlike rhabdomyolysis and neuroleptic malignant syndrome (NMS), massive asymptomatic creatine kinase elevation (MACKE) represents a condition commonly detected during routine screening in patients receiving antipsychotic drugs. In particular, current evidence indicates a greater incidence of this condition in patients without signs of NMS, rhabdomyolysis, or other causes of CK increase during exposure to second-generation antipsychotics (SGAs) than first-generation antipsychotics (FGAs) with a variable onset and duration. Although its pathophysiology is still not fully elucidated, MACKE has usually been recognized as a self-limiting condition, but drug discontinuation might also be required to successfully revert it. Overall, knowledge in this field is mainly extrapolated from adult data, while similar evidence in youths is still limited. As clinicians might often deal with MACKE, its understanding needs to be expanded to avoid misdiagnosis, potentially leading to wasteful healthcare spending and unfavorable patient outcomes. Methods: By reporting the first case of MACKE in an adolescent receiving an SGA, namely paliperidone, we also aimed to provide a comprehensive overview of this medical condition. Conclusions: Making a MACKE diagnosis is essential since its relevant clinical and economic implications are mainly related to unnecessary closer laboratory monitoring or therapeutic changes (e.g., drug discontinuation or switch to another medication).

Autosomal dominant polycystic kidney disease (ADPKD) represents the most common inherited kidney disorder leading to kidney failure in a significant percentage of patients over time. Although previously considered as an adult disease, robust evidence demonstrated that clinical manifestations might occur during childhood and adolescence. Therefore, early identification and treatment of the disease are of cardinal importance for pediatricians to ensure the best long-term outcomes. To date, licensed treatment options are limited but promising potential therapeutic targets are emerging. Among these, an intriguing pathophysiological role for microRNAs as small molecules with a critical role in regulating gene expression has been considered possible in ADPKD. Indeed, numerous circulating microRNAs have been found to be dysregulated in ADPKD, suggesting their potential role as biomarkers and therapeutic targets. Based on this background, further detailed insights into the mechanisms of miRNAs contributing to ADPKD development might pave the way for their effective application as a targeted treatment in young patients with ADPKD. We aimed to summarize the most recent evidence in this fascinating research area, providing a comprehensive overview of the current landscape of specific microRNAs in ADPKD as a potential innovative therapeutic strategy for these young patients.

The role of obesity as a risk factor for chronic kidney disease (CKD) in adulthood has been well established. Over the last years, kidney damage (KD) has emerged as a significant consequence of obesity since childhood. Indeed, a complex interplay of metabolic factors, including insulin resistance (IR), hypertension, oxidative stress, adipose tissue dysfunction, and systemic inflammation, might affect renal hemodynamics, contributing to CKD development over time in at-risk young patients. As the prevalence of pediatric obesity continues to rise globally, understanding the implications for kidney health in terms of early intervention is of paramount importance. Careful monitoring of kidney function within a multidisciplinary approach in children with obesity is crucial for detecting early KD, allowing for timely lifestyle modifications and treatment. In this framework, continued research is essential to further elucidate mechanisms linking obesity and KD and to explore not only effective preventive strategies but also the long-term impact of obesity on kidney health in children with obesity. Given the intimate link of KD with the metabolic milieu in children with obesity, we aimed to provide a comprehensive and insightful overview on KD and its implications in pediatric obesity by reviewing the most recent literature in the field.