Abstract
Hyperuricemia is common in chronic kidney disease (CKD). Hyperuricemia is not only a result of CKD but may also be a cause of incidence and progression of CKD. This scenario composes a chicken and egg problem, which should be resolved by an interventional randomized controlled trial. Until accumulating evidence is available, consensus on the treatment of asymptomatic hyperuricemia in CKD remains to be established. The treatment is first done with nutritional instruction and life-style modification such as reducing alcohol consumption. If insufficient, uric acid lowering drugs will be administered; xanthine oxidase inhibitor or uricosuric agent. In some situation both drugs can be given simultaneously according to the disease type of hyperuricemia which can be simply examined by spot urine. Target range of serum uric acid has not been determined yet but we recommend to be less than 6.5 mg/dL for present in order to inhibit the progression of CKD reaching to end-stage renal disease. Ongoing randomized controlled trials may open a new era of the hyperuricemia in CKD. ABCG2 in the intestine may play a compensatory role in face of decreasing uric acid excretion to urine. The mechanism of the upregulation of ABCG2 in CKD and signal transduction in the cell should be further investigated.
