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Thyroid Disorders and Treatments / Methemoglobinemia and Tumor Lysis Syndrome · Journal article
Frontiers in Endocrinology · August 10, 2026
A consensus or society position rather than new primary data.
This is a narrative review consolidating current knowledge of pediatric hyperuricemia, emphasizing genetic bases (ABCG2 dysfunction, ADTKD variants), metabolic mechanisms (insulin resistance, oxidative stress), and clinical associations with CKD and cardiovascular remodeling. The authors acknowledge that mechanistic associations are primarily supported by adult and experimental data requiring pediatric validation, and provide guidance on management across six clinical scenarios including asymptomatic hyperuricemia, gout, nephrolithiasis, inherited purine disorders, CKD-associated hyperuricemia, and tumor lysis syndrome.
Journal article. Children and adolescents with hyperuricemia; review does not report original research population..
ABCG2 dysfunction, ADTKD-UMOD, and ADTKD-REN contribute to early-onset hyperuricemia, gout, nephrolithiasis, and renal involvement Obesity-related insulin resistance may promote urate accumulation through oxidative stress, endothelial dysfunction, and inflammasome activation Persistent uric acid elevation associated with chronic kidney disease progression, elevated blood pressure, and subclinical cardiovascular remodeling
Specific dosing, monitoring, and safety data for pediatric pharmacological treatments not detailed in provided abstract
Clinicians should recognize that asymptomatic serum urate elevation is often the first presentation in children, whereas nephrolithiasis, gout, renal dysfunction, or acute hyperuricemia should prompt evaluation for underlying genetic, metabolic, renal, or treatment-related causes. Early identification and personalized intervention are emphasized to prevent long-term renal and metabolic complications, though the evidence base for many pediatric-specific recommendations remains incomplete.
A comprehensive narrative review synthesizing current understanding of pediatric hyperuricemia genetics, mechanisms, and clinical management, intended to inform clinical practice and identify evidence gaps rather than report original research findings.
Clinicians should recognize that asymptomatic serum urate elevation is often the first presentation in children, whereas nephrolithiasis, gout, renal dysfunction, or acute hyperuricemia should prompt evaluation for underlying genetic, metabolic, renal, or treatment-related causes. Early identification and personalized intervention are emphasized to prevent long-term renal and metabolic complications, though the evidence base for many pediatric-specific recommendations remains incomplete.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Hyperuricemia (HUA) is a heterogeneous group of metabolic disorders caused by long-term disturbances in purine metabolism. In recent years, although adult HUA and gout have been extensively studied, the understanding of HUA and gout in children and adolescents remains insufficient. Diagnostic criteria for adult HUA are well-established, but no consensus has yet been reached regarding its definition in children and adolescents. This review summarizes the current understanding of pediatric HUA, emphasizing its genetic basis, metabolic mechanisms, and clinical associations. ATP-binding cassette subfamily G member 2 (ABCG2) dysfunction, gene-defined forms of autosomal dominant tubulointerstitial kidney disease (ADTKD), particularly ADTKD-UMOD and ADTKD-REN, and selected purine metabolism disorders contribute to early-onset HUA, gout, nephrolithiasis, and renal involvement. Obesity-related insulin resistance (IR) may promote urate accumulation through pathways linked to oxidative stress, endothelial dysfunction, and inflammasome activation. Persistent elevation of uric acid (UA) has been associated with chronic kidney disease (CKD) progression, elevated blood pressure (BP), and subclinical cardiovascular remodeling. However, many of these mechanistic associations are supported primarily by adult and experimental studies and require further validation in children. We also review non-pharmacological management and indication-based pharmacological treatment strategies for pediatric HUA. These indications include asymptomatic hyperuricemia (AH), pediatric gout, UA nephrolithiasis, inherited purine metabolism disorders, CKD-associated HUA, and tumor lysis syndrome (TLS)-associated acute HUA, with emphasis on pediatric evidence, regulatory approval, off-label use, dosing, monitoring, and safety. In children, asymptomatic serum urate elevation is often the first recognized presentation, whereas nephrolithiasis, gout, renal dysfunction, or acute HUA should prompt evaluation for genetic, metabolic, renal, or treatment-related causes. These findings underscore the need for early identification and personalized intervention in children with HUA to prevent long-term renal and metabolic complications.
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