Does uric acid have a pathogenetic role in graft dysfunction and hypertension in renal transplant recipients?

Armstrong, Kirsten A., Johnson, David W., Campbell, Scott B., Isbel, Nicole M. and Hawley, Carmel M. (2005) Does uric acid have a pathogenetic role in graft dysfunction and hypertension in renal transplant recipients?. Transplantation, 80 11: 1565-1571. doi:10.1097/01.tp.0000183895.88572.13


Author Armstrong, Kirsten A.
Johnson, David W.
Campbell, Scott B.
Isbel, Nicole M.
Hawley, Carmel M.
Title Does uric acid have a pathogenetic role in graft dysfunction and hypertension in renal transplant recipients?
Journal name Transplantation   Check publisher's open access policy
ISSN 0041-1337
1534-6080
Publication date 2005-12-15
Year available 2005
Sub-type Article (original research)
DOI 10.1097/01.tp.0000183895.88572.13
Open Access Status
Volume 80
Issue 11
Start page 1565
End page 1571
Total pages 7
Place of publication Philadelphia, PA, United States
Publisher Lippincott Williams and Wilkins
Language eng
Subject 110312 Nephrology and Urology
Abstract Background. Uric acid (UA) may play a pathogenetic role in hypertension and kidney disease. We explored the prevalence of hyperuricemia and the relationship of UA to graft function and hypertension in prevalent renal transplant recipients (RTR).
Formatted abstract
Background. Uric acid (UA) may play a pathogenetic role in hypertension and kidney disease. We explored the prevalence of hyperuricemia and the relationship of UA to graft function and hypertension in prevalent renal transplant recipients (RTR).

Methods. Baseline and follow-up data were collected on 90 RTR (mean age 51 yrs, 53% male, median transplant duration 7 years). Graft function was estimated using MDRD Study Equation 7.

Results. At baseline, 70% RTR had hyperuricemia (UA >7.0 mg/dl (0.42mmol/L) in men and >6.0 mg/dl (0.36 mmol/L) in women) compared to 80% after 2.2 years (P=0.06). UA was not associated with blood pressure (BP) level but was higher in RTR with a history of hypertension compared to those without (8.6+/-1.8 vs. 7.3+/-2.2 mg/dl, [0.51+/-0.11 vs. 0.43+/-0.13 mmol/L], P=0.003) and in RTR on >=3 antihypertensive medications compared to those taking less (9.1+/-1.6 vs. 7.6+/-1.8 mg/dL, [0.54+/-0.1 vs. 0.45+/-0.11 mmol/L], P<0.001). A history of hypertension was independently predictive of UA ([beta] 0.06, [95% CI 0.02 to 0.10], P=0.007) in addition to sex, cyclosporine dose, prednisolone dose, estimated glomerular filtration rate (eGFRMDRD) and beta-blocker therapy. UA was independently predictive of follow-up eGFRMDRD ([beta] -22.2 [95% CI -41.2 to -3.2], P=0.02) but did not predict change in eGFRMDRD over time. UA was independently associated with requirement for antihypertensive therapy ([beta] 0.34, [95% CI 1.05 to 1.90], P=0.02).

Conclusions. Hyperuricemia is common in RTR and is associated with need for antihypertensive therapy and level of graft function.
Keyword Hyperuricemia
Hypertension
Renal transplantation
Graft dysfunction
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Medicine Publications
 
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Created: Tue, 07 Jul 2009, 01:38:13 EST by Maria Campbell on behalf of Faculty Of Health Sciences