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FRI0318 Serum URIC Acid as an Independent Risk Factor on Progression of Chronic Kidney Disease in Gout Patients with URIC Acid Lowering Agent
  1. E.-J. Park1,
  2. E.Y. Hee2,
  3. S. Lee2,
  4. J. Hwang3,
  5. E.-J. Kwon4,
  6. J. Kim1,
  7. E.-M. Koh2
  1. 1Department of Medicine, Jeju National University Hospital, Jeju
  2. 2Department of Medicine, Samsung Medical Center
  3. 3Department of Medicine, Kangbuk Samsung Hospital, Seoul
  4. 4Jeju National University Hospital, Jeju, Korea, Republic Of

Abstract

Background Hyperuricemia is particularly common in patients with chronic kidney disease (CKD). Its role, however, as a risk factor for renal outcomes of CKD is debated and those data in gout patients with CKD are rare.

Objectives This aim of study was to evaluate long-term effect of serum uric acid (SUA) level on progression of CKD in gout patients with uric acid lowering treatment.

Methods All patients who had a first visit for gout with CKD at Samsung Medical Center between 1995 and 2003, and follow-up until December 2012 or expired during follow-up period were included and retrospective analyzed. CKD was defined as an estimated glomerular filtration rate GFR) of <60 mL/min/1.73m2 via the Modification of Diet in Renal Disease Study equation more than 3 months according to the Kidney Disease Outcome Quality Initiative CKD classification. All serum creatinine and matched SUA taken during follow-up period were analyzed by using mixed effect model to determine the effect of SUA level on renal outcome.

Results One-hundred eleven gout patients with CKD were observed. The mean age of the patients at diagnosis of gout was 51.3 and mean follow-up duration was 13 years. Baseline estimated GFR and serum creatinine were 47.7 mL/min/1.73m2 and 1.62 mg/dL, respectively. Eight (7.2%) patients revealed CKD stage 4 and the rest of patients (92.8%) were CKD stage 3. Maintaining the SUA below 6 mg/dL showed protective effect on serum creatinine and estimated GFR compared with maintaining SUA more than 6 mg/dL (p <0.0001 and p =0.02, respectively). The elevation of SUA as a continuous variable was also related to poor renal outcome in gout patients with CKD (p <0.0001). This effect of SUA on progression of CKD was not changed after adjusting for duration of gout and age at baseline, time-dependent hypertension, diabetes mellitus, hyperlipidemia, obesity, intrinsic renal diseases, and obstructive renal diseases. In particular, for every 1 mg/dL increase of the SUA, serum creatinine revealed to be increased by 0.019 mg/dL in group with SUA more than 6 mg/dL. Hypertension, diabetes mellitus and intrinsic renal disease were independent risk factors for progression of CKD in gout patients (p <0.0001, p <0.0001 and p =0.014, respectively).

Conclusions Our long term follow-up data demonstrated the SUA level was independent risk factor for progression of CKD in gout patients with uric acid lowering treatment. Maintaining of SUA level below 6 mg/dL would be essential to protect renal function in gout patients with CKD.

Disclosure of Interest None declared

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