Hyperuricemia and Urologic Disease

Abstract

Gout is a disease that causes painful inflammatory arthritis related to hyperuricemia, due to the incorrect metabolism of uric acid. Decreased renal excretion of urate is thought to be the major hyperuricemic mechanism. Most genes responsible for the serum uric acid (SUA) level encode uric acid transporters or related regulatory proteins. The acquired effects can also modulate SUA level and uric acid excretion, which can result in acute gout. Interestingly, kidney related comorbidities in gout, such as hypertension, chronic kidney disease (CKD), and urolithiasis, all have a fairly high prevalence. Recent advancements in genetics and molecular physiology have greatly improved our understanding of renal reabsorption and secretion of filtered uric acid. Furthermore, the baseline SUA level appears to be established by a net balance between absorption and secretion through the epithelium of the kidneys and intestines. There have also been considerable progress in the management of gout patients with CKD. Increased prevalence of gout with CKD can be balanced by an expanded spectrum of treatment options for this important disease. Another issue is that lowering of the uric acid level can reduce the incidence of cardiovascular disease, renal disease, and urological complications. Basic research and clinical studies on these mechanisms might be helpful in determining the appropriate treatment for hyperuricemic patients. Based on currently existing literature, there have been improvements associated with medications that lower uric acid, particularly xanthine oxidase inhibitors. Here, we review the pathogenesis and epidemiology of hyperuricemia, specific diseases related to uric acid, and up-to-date perspectives on their management.