A sugar transporter regulates serum urate levels: implications for prevention and management of hyperuricemia in gout.

摘要

Introduction: Gout is increasing in prevalence in the United States. More patients with refractory tophaceous disease are being seen, including older patients and those with multiple comorbidities such as diabetes, hypertension, chronic kidney disease, and congestive heart failure. There is also growing but as yet unresolved evidence for the potential of hyperuricemia to directly impact on blood pressure and cardiovascular diseases. New treatments, such as febuxostat and pegloticase, are emerging for refractory hyperuricemia. However, in most gout patients hyperuricemia is caused by long-standing renal underexcretion of uric acid, an abnormality that is often precipitated or exacerbated by diuretic therapy, insulin resistance, hypertension, and development of even moderate degrees of renal insuffi ciency [1]. This scenario points to opportunities to intervene at the level of both prophylaxis and treatment of hyperuricemia by more advanced uricosuric therapies. This will be aided by recent clinical-translational advances in understanding renal uric acid disposition.