title: Hyperuricemia influences chronic cyclosporine nephropathy.
abstract: BACKGROUND
  The observation that long-standing hyperuricemia is associated with chronic tubulointerstitial disease, afferent arteriolopathy, intrarenal vasoconstriction, and increased vascular resistance raises the hypothesis that hyperuricemia might contribute to chronic cyclosporine (CsA) nephropathy. The aim of the present study was to investigate the effect of hyperuricemia on chronic CsA nephropathy.
  
  
  METHODS
  Patients who were treated with CsA-based immunsuppressive regimens and underwent a renal biopsy were enrolled in this case-control study. We retrospectively obtained posttransplant baseline serum creatinine, uric acid (UA), mean serum UA, and creatinine values 3 months prior to biopsy. CsA trough levels, mean blood pressure, diuretic and antihypertensive treatment were recorded. Biopsy specimens showing CsA nephropathy (n = 34) were revaluated by a pathologist to score CsA nephropathy according to recent quantitative criteria for calcineurin inhibitor arteriolopathy as proposed by M.J. Mihatsch.
  
  
  RESULTS
  As compared with the non-CsA nephropathy group, recipient and donor ages, donor origin and cold ischemia times were similar for the CsA nephropathy group (P > .05). Mean CsA doses, CsA trough (C(0)), and C(2) levels were not different between the groups (P > .05). Systolic and diastolic blood pressure, glomerular filtration rate, diuretic usage, and antihypertensive treatment were also similar in CsA nephropathy and non-CsA nephropathy groups (P > .05). Mean serum UA level within 3 months prior to biopsy in the CsA nephropathy and non-CsA nephropathy groups were 7.5 +/- 1.4 mg/dL versus 5.7 +/- 1.4 mg/dL, respectively (P < .001).
  
  
  CONCLUSIONS
  Hyperuricemia seems to exacerbate CsA-induced nephropathy.
authors.affiliation: Department of Nephrology, Dokuz Eylul University, School of Medicine, Balcova, Izmir. funda.saglam@dcu.edu.tr
authors.forename: F
authors.initials: F
authors.lastname: Saglam
authors.forename: A
authors.initials: A
authors.lastname: Celik
authors.forename: S
authors.initials: S
authors.lastname: Sarioglu
authors.forename: C
authors.initials: C
authors.lastname: Cavdar
authors.forename: A
authors.initials: A
authors.lastname: Sifil
authors.forename: H
authors.initials: H
authors.lastname: Gulay
authors.forename: T
authors.initials: T
authors.lastname: Camsari
mesh_terms: D000328:Adult; D000959:Antihypertensive Agents / Q000627:therapeutic use; D002908:Chronic Disease; D016572:Cyclosporine / Q000009:adverse effects*; D005260:Female; D006801:Humans; D033461:Hyperuricemia / Q000209:etiology / Q000503:physiopathology*; D007166:Immunosuppressive Agents / Q000009:adverse effects; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D014527:Uric Acid / Q000097:blood
chemical_list: D000959:Antihypertensive Agents; D007166:Immunosuppressive Agents; D014527:Uric Acid; D016572:Cyclosporine