ABCG2 and metabolic syndrome: Mutated or dysfunctional ABCG2 may lead to significantly reduced excretion, moderate hyperuricemia and metabolic syndrome.139 Initially, it was hypothesized that the loss or reduction of ABCG2-mediated renal urate secretion would result in increased renal urate reabsorption, as diminished renal excretion is typically considered the primary mechanism of hyperuricemia in most gout patients.