A new classification for gout is proposed in an article published in this week’s Nature Communications. The work describes a mechanism for reduced removal of urate - the culprit for joint inflammation associated with gout - implicating a dysfunctional urate exporter channel in this process. Reclassification of disease subtypes may enable accurate identification of the cause of abnormal level of urate and could provide a more effective therapeutic strategy.
A common feature of gout is hyperuricemia (elevated blood urate levels) that is clinically classified as either urate overproduction, underexcretion by the kidneys, or a combination of both. Although the kidneys are responsible for most of the urate clearance, Kimiyoshi Ichida and colleagues suggest that other excretion pathways should also be considered when classifying the disease. They show that reduced extra-renal removal of urate is misclassified as overproduction type hyperuricemia and recommend that the hyperuricemia types should be reclassified to include extra-renal underexcretion.
The authors find a link between a dysfunctional urate exporter called ABCG2 and decreased extra-renal urate excretion in human patients with hyperuricemia and mouse models of the disease. ABCG2 may, therefore, represent a potential target for urate-lowering treatments.
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