Hyperuricemia acts as an independent risk factor for progression of chronic kidney disease in childrenHigh uric acid levels may drive kidney disease in children

A bidirectional pathogenic interplay exists between pediatric chronic kidney disease (CKD) and hyperuricemia (HUA). Hyperuricemia serves as an independent risk factor for the onset and progression of CKD, while also representing a common complication arising from impaired renal excretory function. Amid the rising global prevalence of pediatric CKD and growing evidence implicating metabolic disturbances in renal injury, the reciprocal pathological mechanisms underlying uric acid–mediated kidney damage have emerged as a critical research focus. Elevated serum uric acid induces renal tubulointerstitial injury through oxidative stress, systemic inflammatory cascades, and endothelial dysfunction. Conversely, diminished uric acid excretion resulting from CKD further aggravates hyperuricemia, establishing a self-perpetuating vicious cycle. However, epidemiological evidence specific to the pediatric population remains limited, and current clinical management strategies are largely extrapolated from adult studies, lacking evidence-based guidelines tailored to the unique growth and developmental characteristics of children. This review systematically summarizes the epidemiological features, molecular pathogenic mechanisms, clinical implications, and therapeutic approaches for HUA comorbid with pediatric CKD. We specifically highlight uric acid–driven renal injury pathways, the accelerating effect of HUA on CKD progression, and age-specific challenges in pediatric diagnosis and standardized intervention. By integrating recent advances in preclinical and clinical research, this review aims to provide a theoretical foundation for the early screening, timely diagnosis, and individualized standardized management of hyperuricemia in children with CKD.