Gout is an inflammatory disease that results from the deposition of uric acid crystals in the joints. It tends to be somewhat common in people with high levels of uric acid in the blood, which is, in turn, often the result of reduced renal excretion of the acid. How does this chain of events come about? Two papers in Nature Genetics give us a clue: Veronique Vitart and her colleagues and Angela Doring and her colleagues independently identified variants in the gene SLC2A9 that are linked to variability in uric acid concentrations.

SLC2A9 encodes a fructose transporter, but Vitart and colleagues found that the protein can also transport uric acid when expressed in Xenopus oocytes. Moreover, the transporter was already known to be expressed in the kidney. So, this molecule could very well turn out to be a therapeutic target for gout. The image below, from Ed Euthman, shows uric acid crystals in a human joint.