Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary renal disorder and primarily arises from mutations in either the polycystic kidney disease 1 (PKD1) or 2 (PKD2) gene. Although traditionally categorized as an adult-onset disease, cystogenesis often begins in utero, and structural changes may become evident during childhood. Although most pediatric patients with ADPKD remain asymptomatic, hypertension occurs in 20%–40% of cases, and albuminuria may also be present. Both findings represent early, treatable manifestations that can significantly influence long-term prognosis. Ultrasonography is the preferred diagnostic modality; however, genetic testing is indicated in very-early-onset or atypical cases. The cornerstone of disease management is rigorous blood pressure control using renin–angiotensin system inhibitors, along with lifestyle modifications such as sodium restriction and adequate hydration. Early diagnosis and intervention are essential for optimizing long-term clinical outcomes in pediatric patients with ADPKD. This study aimed to provide a comprehensive review of the genetics, pathophysiology, clinical manifestations, diagnosis, treatment, and future management of pediatric ADPKD.

The worldwide incidence of precocious puberty, which is associated with negative health outcomes, is increasing. Several studies have suggested that environmental factors contribute to the development of precocious puberty alongside genetic factors. Some epidemiological studies have provided limited evidence suggesting an association between exposure to air pollution and changes in pubertal development. This systematic review aimed to summarize existing evidence on the association between air pollution exposure and precocious puberty. Following the Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines, we searched two databases (PubMed and Web of Science) until August 2023. The included studies assessed the association between air pollutant exposure and the risk of precocious puberty, early menarche, or pubertal development. Two authors independently performed study selection and data extraction. A meta-analysis and analysis of the risk of bias were infeasible due to the limited number of studies and the heterogeneity among them. The literature search resulted in 184 studies, from which we included six studies with sample sizes ranging from 437 to 4,074 participants. The studies reported heterogeneous outcomes. Four studies found that increased exposure to air pollution was related to earlier pubertal onset. One study was inconclusive, and another suggested that air pollutant exposure may delay the onset of thelarche. Most studies suggest that exposure to air pollutants accelerates pubertal development; however, the results from the available studies are inconsistent. More extensive and well-designed longitudinal studies are required for a comprehensive understanding of the association between air pollution and precocious puberty.