Dr Kimiyoshi Ichida and colleagues, from Tokyo University, identified a new mechanism for the elevated blood urate levels that cause the joint inflammation associated with gout.
They identified a protein linked to lower urate removal from areas outside the kidneys.
Lack of knowledge of this process has meant that impaired removal of urate from areas outside the kidneys has been misclassified as overproduction of urate.
The researchers believe that, although most urate is cleared by the kidneys, these other pathways must also be considered when classifying gout. They recommend that gout subtypes should be reclassified to include extra-renal underexcretion as a cause of abnormal urate levels.
A reclassification of gout along these lines may allow accurate identification of the cause of abnormal urate levels and lead to more effective therapy, the researchers believe.
Dr Ichida and colleagues found a link between dysfunctioning of the urate exporter channel ABCG2 and reduced urate excretion from the kidneys in both mice and human patients with hyperuricemia. They believe that the ABCG2 channel could be a useful target for gout treatments focused on lowering urate levels.