fig1

Figure 1. Pathological effects of hyperuricemia on kidney structure and function. Pathophysiology of uric acid - mediated kidney damage. Uric acid enters renal tubular cells through a specific transporter, urate transporter 1 (URAT-1), and two generic transporters, organic anion transporter 4 (OAT-4) and OAT-10. On the basolateral site, the glucose transporter 9 (GLUT-9) is the principal transporter responsible for extrusion of uric acid into circulation. Hyperuricemia might cause hemodynamic effects including increased activity of the RAAS, increased production and activity of vasoconstrictors, such as ET-1, Ang II and thromboxane, and impairment in nitric oxide (NO) availability. These changes lead to impaired endothelium-dependent relaxation and endothelial dysfunction, with negative consequence on kidney structure and function. Moreover, uric acid has been demonstrated to have cellular effects inducing oxidative stress, inflammation and cellular phenotype transition, contributing to glomerulosclerosis and interstitial fibrosis. RAAS: renin angiotensin aldosterone system; NO: nitric oxide; GLUT: glucose transporter; URAT: urate transporter; OAT: organic anion transporter.