The role of uric acid in chronic kidney disease patients

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Hyperuricaemia is strongly linked with chronic kidney disease (CKD) and may be caused by impaired excretion due to low glomerular filtration rate (GFR), or may reflect increased cellular breakdown or local hypoxia in renal disease.1 Accumulating evidence shows that high uric acid (UA) levels might also have a pathologic role in the progression of CKD, rather than only be a reflection of reduced renal clearance of uric acid.3 In addition to impaired endothelial nitric oxide production with endothelial dysfunction, other underlying mechanisms that have been proposed include insulin resistance, activation of renin‐angiotensin system, increased interleukin‐6 synthesis and vascular atherosclerosis.4 A number of inconsistent results have also been reported in terms of the role of uric acid in the initiation and progression of CKD.8
A further issue that remains to be resolved is the contribution of hyperuricaemia to cardiovascular risk. Recent studies have shown hyperuricaemia to be linked with cardiovascular events and patient mortality in patients with congestive heart failure and CKD, as well as in the general population.12 There have also been studies on predialysis patients or those undergoing haemodialysis concluding that uric acid level was independently related with mortality in a J‐shaped relationship.14 Therefore, the influence of uric acid on vascular damage has been suggested to continue, even after the commencement of renal replacement therapy.
Serum uric acid levels may vary to a large extent over time, especially after dietary or pharmacologic intervention. However, most published studies evaluating the relationship between uric acid level and kidney or cardiovascular outcomes use only one measurement of uric acid at baseline as the determinant to predict events several years in the future.16 In the present study, we investigated the clinical outcomes in relation to uric acid levels, which were assessed by the mean values of the first two consecutive measurements during the study period in stage 3–5 CKD patients.
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