title: Uric acid and allograft loss from interstitial fibrosis/tubular atrophy: post hoc analysis from the angiotensin II blockade in chronic allograft nephropathy trial.
abstract: BACKGROUND
  Uric acid has been linked to the progression of native kidney disease. Studies evaluating its contribution to allograft function in kidney transplant recipients, among whom hyperuricemia is common, have yielded mixed results.
  
  
  METHODS
  We evaluated the association between baseline uric acid and the primary composite outcome of doubling of interstitium or ESRD from interstitial fibrosis and tubular atrophy (IF/TA) in the Angiotensin II Blockade for Chronic Allograft Nephropathy (ABCAN) Trial participants. Subjects underwent uric acid, iothalamte GFR, and urine albumin to creatinine (ACR) measurements annually for 5 years in addition to an allograft biopsy at baseline and 5 years.
  
  
  RESULTS
  Baseline uric acid was 5.57±1.48 mg/dL; male sex, higher BMI, diuretic use, and lower GFR were associated with higher uric acid, whereas older age, less than 3 HLA matches and having a female donor were associated with lower levels. In multivariate analysis adjusting for baseline GFR, uric acid was associated with doubling of interstitium or ESRD from IF/TA (OR 1.83, 95% CI, 1.06-3.17, P=0.03). Over time, a 1 mg/dL increase in time-varying uric acid was associated with a 2.39 mL/min lower final GFR (P<0.001) but not with the secondary outcome of creatinine doubling, ESRD, or death.
  
  
  CONCLUSIONS
  These data suggest that uric acid is associated with IF/TA and thus may be a viable target for intervention.
authors: 1 Division of Renal Diseases and Hypertension, University of Minnesota, Minneapolis, MN. 2 Nephrology Division, Hennepin County Medical Center, Minneapolis, MN. 3 Department of Pediatrics, University of Minnesota, Minneapolis, MN. 4 Department of Pathology, University of Washington, Seattle, WA. 5 Department of Surgery, University of Minnesota, Minneapolis, MN. 6 Address correspondence to: Hassan N. Ibrahim, M.D., MS, Director, Division of Renal Diseases and Hypertension, University of Minnesota, 717 Delaware St. SE, Suite 353, MDC 1932, Minneapolis, MN 55414.
authors: Allyson
authors: A
authors: Hart
authors: Scott
authors: S
authors: Jackson
authors: Bertram L
authors: BL
authors: Kasiske
authors: Michael S
authors: MS
authors: Mauer
authors: Behzad
authors: B
authors: Najafian
authors: Arthur J
authors: AJ
authors: Matas
authors: Richard
authors: R
authors: Spong
authors: Hassan N
authors: HN
authors: Ibrahim
mesh_terms: D064591:Allografts; D000804:Angiotensin II / Q000187:drug effects*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000008:administration & dosage*; D001284:Atrophy; D001706:Biopsy; D002908:Chronic Disease; D003404:Creatinine / Q000652:urine; D018450:Disease Progression; D004311:Double-Blind Method; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000187:drug effects / Q000502:physiology; D006084:Graft Rejection / Q000150:complications / Q000378:metabolism* / Q000517:prevention & control; D006801:Humans; D033461:Hyperuricemia / Q000097:blood* / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000601:surgery; D016030:Kidney Transplantation; D007684:Kidney Tubules / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009395:Nephritis, Interstitial / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D016896:Treatment Outcome; D014527:Uric Acid / Q000097:blood*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000804:Angiotensin II; D014527:Uric Acid; D003404:Creatinine