ScholarWorks@중앙대학교

초록

Chronic kidney disease (CKD) affects approximately 10-15% of adults globally and is a significant public health issue owing to its association with cardiovascular disease, end-stage kidney disease, and high healthcare costs. Hyperuricemia has emerged as an important modifiable risk factor influencing CKD progression. Elevated uric acid (UA) levels contribute to kidney injury through crystaldependent mechanisms, including monosodium urate crystal deposition and NLRP3 inflammasome activation, and crystal-independent pathways, such as endothelial dysfunction, activation of the renin-angiotensin-aldosterone system, and oxidative stress. Observational studies have consistently linked hyperuricemia to an increased risk of CKD onset and accelerated disease progression. Nevertheless, randomized controlled trials and meta-analyses investigating UA-lowering therapy (ULT) for asymptomatic hyperuricemia have yielded conflicting results regarding its effectiveness in slowing CKD progression. Clinical guidelines also differ: Japanese guidelines recommend ULT for serum UA levels exceeding 8.0 mg/dL, whereas Western guidelines generally do not support routine treatment of asymptomatic hyperuricemia. Thus, there remains a clear need for large-scale, long-term studies to define patient subgroups most likely to benefit from ULT and guide individualized treatment approaches.

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