title: Improvement of renal function in patients with chronic gout after proper control of hyperuricemia and gouty bouts.
abstract: OBJECTIVE
  To evaluate the effect of nonsteroidal anti-inflammatory drug (NSAID) withdrawal on renal function in patients with chronic gout after proper control of hyperuricemia and gouty symptoms.
  
  
  METHODS
  Patients with chronic gout, who regularly used NSAIDs to control gouty symptoms prior to urate-lowering therapy, were prospectively followed up in an observational study. Risk factors for renal function impairment were recorded, and the clearance of creatinine (Ccr) was initially measured while on colchinine therapy to prevent gouty bouts. Therapy with urate-lowering drugs was started in order to keep serum urate levels under 6.0 mg/dl (275 micromol/l), and the Ccr was monitored during the follow-up period. Final assessment of the renal function was made after 1 year free from gouty bouts and without NSAID therapy during this period.
  
  
  RESULTS
  87 patients completed a 1-year period of NSAID withdrawal. Low initial Ccr was related to age, hypertension, hypertriglyceridemia and the presence of previous renal diseases. After proper control of gout and NSAID withdrawal during 1 year, the mean Ccr significantly raised from 94 to 104 ml/min. The improvement was especially significant in patients whose initial Ccr was under 80 ml/min. Their mean Ccr rose from 60 to 78 ml/min, and 12 of 29 patients achieved normal Ccr at the end of the study. No risk factor correlated with improvement of the renal function.
  
  
  CONCLUSIONS
  Renal function impairment in patients with chronic gout is mainly related to vascular risk factors, but improvement of the renal function was observed after proper control of hyperuricemia and NSAID withdrawal. Optimal control of hyperuricemia and, therefore, of symptoms of gout should be especially considered in patients with vascular risk factors in order to avoid renal function loss due to NSAID use.
authors.affiliation: Rheumatology Section, Hospital de Cruces, Barakaldo, Spain. fperez@hcru.osakidetza.net
authors.forename: F
authors.initials: F
authors.lastname: Perez-Ruiz
authors.forename: M
authors.initials: M
authors.lastname: Calabozo
authors.forename: A M
authors.initials: AM
authors.lastname: Herrero-Beites
authors.forename: G
authors.initials: G
authors.lastname: García-Erauskin
authors.forename: J I
authors.initials: JI
authors.lastname: Pijoan
mesh_terms: D000328:Adult; D000368:Aged; D000493:Allopurinol / Q000008:administration & dosage; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000009:adverse effects*; D001553:Benzbromarone / Q000008:administration & dosage; D003404:Creatinine / Q000097:blood; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D006073:Gout / Q000097:blood / Q000188:drug therapy*; D006074:Gout Suppressants / Q000008:administration & dosage; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D051437:Renal Insufficiency / Q000139:chemically induced* / Q000453:epidemiology / Q000517:prevention & control*; D012307:Risk Factors; D014527:Uric Acid / Q000097:blood*; D014528:Uricosuric Agents / Q000008:administration & dosage
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D006074:Gout Suppressants; D014528:Uricosuric Agents; D014527:Uric Acid; D001553:Benzbromarone; D000493:Allopurinol; D003404:Creatinine