Uric Acid and Renal Function

نویسندگان

  • Guilherme Ambrosio Albertoni
  • Fernanda Teixeira
  • Nestor Schor
چکیده

Since the discovery of hyperuricemia as the cause of gout in the early 1800s, hypertension, cardiovascular disease and kidney disease have also been related to increased serum uric acid (UA) levels in subsequent years (Nakagawa et al., 2006); patients with gout had a much higher prevalence of hypertension (25-50%), mild-to-moderate kidney disease (20-60%) (Kutzing & Firestein, 2008) and cardiovascular disease (90%) compared to the general population. However, conflicting results regarding the role of UA as the causative factor in diseases other than gouty arthritis resulted in a shift of interest away from UA. In recent years, uric acid regained the lost popularity due to new findings in a number of disease states including hypertension, renal disease, metabolic syndrome and many more (Feig et al., 2008). Hyperuricemia arises from excess dietary purine or ethanol intake, decreased renal excretion of UA, or from tumor lyses in lymphoma, leukaemia, or solid tumours (Kutzing & Firestein, 2008). Finally, several drugs alter UA handling by the kidney, for example drug therapy with candesartan (Li et al., 2008) or both loopand thiazide diuretics, all of which increase the net urate reabsorption (Suliman et al., 2006). In the majority of individuals, hyperuricemia will be asymptomatic, but as UA tends to precipitate in tissues and in other body fluids, persistent hyperuricemia may eventually lead to the accumulation of urate crystals in many places, resulting in either acute painful conditions, like gout/tophaceous gout/gouty arthritis, urolithiasis, or, in severe cases, like tumor lysis syndrome, in acute UA nephropathy (Riegersperger et al., 2011). In recent years, increased fructose intake, particularly via sweetened beverages, started to attract more attention from the medical community. During the last two centuries, at least in the western world, dietary fructose intake dramatically increased, with corresponding increases in serum UA levels (Feig et al., 2008). The increase in fructose intake and hyperuricemia is now being associated to the development of metabolic syndrome. Hyperuricemia is associated with an increased risk for developing CKD (Obermayr et al., 2008) and a risk factor for renal dysfunction in patients with rheumatoid arthritis (Daoussis et al., 2009). Retrospective data suggest an influence of hyperuricemia on graft loss after kidney transplantation (Haririan et al., 2010). A screening among 18,020 individuals with chronic kidney diseases (CKD) found a 20.6% prevalence of hyperuricemia. A cross-sectional study in individuals aged over 40 years found 10.5% prevalence of CKD, and among these, 26% were hyperuricemic (Shan et al., 2010). A

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تاریخ انتشار 2012