For decades, the management of hyperuricemia has been largely driven by the occurrence of gout. Outside the context of crystal-induced disease, asymptomatic hyperuricemia has traditionally been regarded just as a biochemical abnormality rather than a clinical and therapeutic target. Consequently, most international guidelines recommend against initiating urate-lowering therapy (ULT) solely to reduce serum uric acid (SUA) concentrations in patients without gout or nephrolithiasis[1]. This conservative approach reflects the lack of good quality evidence and convincing randomized studies demonstrating that lowering SUA translates into reductions in cardiovascular (CV) or renal events[2,3].
