Uric acid (UA) is the end product of purine metabolism in humans due to the loss of uricase activity by various mutations of its gene during the Miocene epoch, which led to humans having higher UA levels than other mammals. Furthermore, 90% of UA filtered by the kidneys is reabsorbed, instead of being excreted. These facts suggest that evolution and physiology have not treated UA as a harmful waste product, but as something beneficial that has to be kept. This has led various researchers to think about the possible evolutionary advantages of the loss of uricase and the subsequent increase in UA levels. It has been argued that due to the powerful antioxidant activity of UA, the evolutionary benefit could be the increased life expectancy of hominids. For other authors, the loss of uricase and the increase in UA could be a mechanism to maintain blood pressure in times of very low salt ingestion. The oldest hypothesis associates the increase in UA with higher intelligence in humans. Finally, UA has protective effects against several neurodegenerative diseases, suggesting it could have interesting actions on neuronal development and function. These hypotheses are discussed from an evolutionary perspective and their clinical significance. UA has some obvious harmful effects, and some, not so well-known, beneficial effects as an antioxidant and neuroprotector.

High uric acid (UA) levels can cause gout, urolithiasis and acute and chronic nephropathy, all of which are due to the deposit of urate crystals. There is also increasing evidence of relationships of hyperuricemia with other important disorders, including hypertension, chronic renal disease, metabolic syndrome and cardiovascular disease, as well as an increased mortality, although a causal relationship between these conditions has not been clearly established. On the other hand, low UA levels are not known to cause any disorder or disease. However, in the last few years a higher prevalence and progression of some neurological diseases have been associated with a low UA, and it is possible that they may predispose to some other disorders, mainly due to the decrease in its antioxidant activity. In this article, the known negative effects of UA are reviewed, as well as the much less-known possible positive actions, and their therapeutic implications.

Objective-To elucidate the real impact in the medical literature of the diVerent denominations for reflex sympathetic dystrophy (RSD). Methods-A

No abstract