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Abstract

There has been a lot of recent excitement regarding elevated serum uric acid as it has been correlated with not just the traditional disorders associated with it, like gout and nephrolithiasis, but also with numerous other chronic diseases like chronic kidney disease, metabolic syndrome, hypertension, coronary artery disease etc which have emerged as the new epidemic of the twenty first century. Although numerous studies have explored the correlation of gout with these lifestyle disorders, none has as yet managed to elucidate the role, if any; hyperuricemia plays in the causation of these. The fact that the rise in mean serum uric acid levels parallels the increase in consumption of certain dietary products has also received a lot of attention. In recent times, light has been shed onto the exact mechanism of renal handling of uric acid, the transporters involved in the tubular excretion and reabsorption, which maintain uric acid homeostasis in our body. We know now that a slight disturbance can overwhelm this machinery and contribute greatly towards the development of hyperuricemia in a given individual. The purpose of this review is to provide a basic understanding into what position this molecule holds in the current clinical scenario and more importantly, how we got here.