european crystal network workshop

    Renoprotective effect of urate lowering therapy in gouty patients with moderate chronic kidney disease

    Background: Approximately 25% of gouty patients suffer from chronic kidney disease (CKD). High serum uric acid (sUA) levels have been related to estimated glomerular filtration-rate (eGFR) imbalance. Beneficial effect of treatment with xanthine oxidase inhibitors (XOI), mostly allopurinol, has already been proved in patients with CKD and asymptomatic hyperuricemia. Although several studies have described the efficacy and renal safety of treatment with XOI in gout, few authors have analyzed its effect on GFR in gouty patients with moderate CKD.

    Objective: To assess the effect of XOI therapy in gouty patients with moderate CKD, in terms of eGFR changes.

    Patients and methods: In this multicenter, retrospective study, we included patients from 4 centers diagnosed with gout (EULAR/ACR criteria) and stage-3 CKD according to Cockroft-Gault formula  (eGFR 30-59 ml/min/m2 ) who received XOI (febuxostat and allopurinol) with a follow-up for 6 and 12 months. We used clinical records to collect patient features (age, sex, body mass index, sUA, hypertension (HTA), diabetes mellitus (DM), dyslipidemia (DL), cardiovascular events), treatments (lipid-lowering drugs, antihypertensives, antidiabetics, antiplatelet therapy, NSAIDs, urate lowering treatments and colchicine) and gout history (duration of disease, tophi presence, clinical and ultrasonographic (US) pattern (monoarticular, oligoarticular, polyarticular). Statistical analysis: descriptive analysis of variables. Mixed effects model lineal regression Differences were considered significant p<0.05.

    Results: 52 patients with gout and  stage-3 CKD were identified. We obtained complete 6 and 12-months follow-up from 37 patients (33 males and 4 females). Mean age was 74.11±6.96 years, 32.4% DM, 83.78 % HTA, 56% DL, 40% tophaceous gout, Clinical and US pattern (37.8% polyarticular, 37.8 oligoarticular and 24.3% monoarticular). Febuxostat 19 patients, Allopurinol 18. Mean baseline sUA was 8.63±1.33 mg/dl, and baseline eGFR was 47.77±8.45 ml/min/m2. To assess the effects of considered variables over eGFR a linear mixed model was adjusted using nlme R-package. Within the adjusted model we obtained significant differences in eGFR between baseline and 6 months (p=0.0081), and between baseline and 12-months (p=0.0028). sUA decreased significantly between baseline and 6 (p=0.0181) and 12 months (p=0.0188).

    Conclusions: Reduction of sUA levels in gouty patients with XOI entitles an improvement of eGFR in stage-3 CKD. These findings suggest that the response to urate lowering therapy take place in the first 6 months, leading to an improvement in eGFR in this period. From 6 months to 1 year, sUA levels are stabilized and so is eGFR.