Abstract
A consistent body of evidence supports an independent association between uric acid (UA) level and the risk of chronic kidney disease (CKD) in humans. It has been observed in experimental data that UA is capable of inducing renal damage through several pathways, including activation of the renin-angiotensin-aldosterone system (RAAS), oxidative stress, and inflammation. Treatment with urate lowering agents and RAAS inhibitors prevented renal insult mediated by UA in animal models. Both of the xanthine oxidase inhibitors available in clinical practice, allopurinol and febuxostat, were efficient in controlling gout flares. However, data from randomised controlled trials are still inconsistent in relation to their benefit for slowing CKD progression. This review discusses the metabolism of urates in humans as well as the experimental and clinical evidence linking UA to CKD. Current evidence about the effect of allopurinol and febuxostat on CKD progression is also considered.
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