Uric acid in diabetic microvascular complications: Mechanisms and therapy
Xin Li, Bo Huang, Yue Liu, Meng Wang, Jingqiu Cui
Abstract
Uric acid (UA) is mainly synthesized in the liver, intestine, and vascular endothelium and excreted by the kidney (70 %) and intestine (30 %). Hyperuricemia (HUA) occurs when UA production exceeds excretion. Many studies have found that elevated UA is associated with diabetic microvascular complications (DMC), including diabetic retinopathy (DR), diabetic nephropathy (DN), and diabetic peripheral neuropathy (DPN). In addition, too high or too low UA levels will promote the occurrence and development of chronic diseases, but the relationship between UA and diabetic microvascular complications (DMC) is not clear. Therefore, the rational treatment of UA in patients with diabetes is essential. In this review, we summarize and discuss the mechanism and treatment of UA and DMC and may provide potential advice for rational drug selection. • SUA was closely related to diabetes and its complications. • Sodium-glucose cotransporter 2 (SGLT-2) could reduce the levels of SUA. • Dotinurad is a newer urate-lowering agent that suppresses UA reabsorption through the selective inhibition of URAT1 in the proximal renal tubules.