Context:In human beings, uric acid is the poorly soluble circulating end product of the purine nucleotide metabolism. A reduction in the glomerular filtration rate (GFR) contributes to hyperuricemia, which is frequently observed in patients with chronic kidney disease (CKD).Evidence Acquisition:Hyperuricemia is defined as a serum uric acid level > 7.0 mg/dL in males and > 6.0 mg/dL in females, while CKD is defined as kidney damage or a GFR < 60 mL/min/1.73 m2 for 3 months or more, irrespective of the cause. Hyperuricemia is common in CKD and may occur because of decreased excretion, increased production, or a combination of both mechanisms.Results:The causes for hyperuricemia in overproducers may be either exogenous or endogenous. CKD has become a global public health problem because of its high prevalence and the accompanying increase in the risk of end-stage renal disease, cardiovascular disease, and premature death. The most common risk factors for CKD are obesity and the metabolic syndrome, which is strongly associated with hyperuricemia probably as a consequence of insulin resistance and the effects of insulin to reduce the urinary urate excretion. For recurring bouts of hyperuricemia or gout, patients should have a blood test and joint fluid test to determine whether the medication taken is effective. Interventional studies are a useful clinical research tool in clarifying the role of hyperuricemia in CKD.Conclusions:Although many evidence-based studies have suggested that uric acid itself may harm patients with CKD by increasing inflammation and CKD progression, the issue is still a matter of controversy. Special attention should be paid to specific contraindications to certain drugs and the possibility of infectious arthritis.
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