Hyperuricemia after renal transplantation

Gores, P. F.; Fryd, David S.; Sutherland, David E.R.; Najarían, John S.; Simmons, Richard L.

doi:10.1016/s0002-9610(88)80196-x

Cited by 73 publications

(66 citation statements)

References 11 publications

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“…134,135 The impact of HUA on graft survival is controversial. Some studies indicate that HUA is only a marker of graft dysfunction, [136][137][138][139] whereas some other studies suggest that UA is an independent risk factor for graft dysfunction. [140][141][142][143][144][145][146] Recently, Hart et al 147 reported that HUA correlated with tubular atrophy and interstitial fibrosis in chronic allograft nephropathy.…”

Section: Hua and Renal Transplantationmentioning

confidence: 99%

Hyperuricemia and chronic kidney disease: an enigma yet to be solved

et al. 2014

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The role of uric acid (UA) on the pathogenesis and progression of chronic kidney disease (CKD) remains controversial. Experimental and clinical studies indicate that UA is associated with several risk factors of CKD including diabetes, hypertension, oxidative stress, and inflammation and hyperuricemia could be considered as a common dominator linking CKD and cardiovascular disease. Notably, the impact of serum UA levels on the survival of CKD, dialysis patients, and renal transplant recipients is also a matter of debate, as there are conflicting results from clinical studies. At present, there is no definite data whether UA is causal, compensatory, coincidental or it is only an epiphenomenon in these patients. In this article, we attempt to review and elucidate the dark side of this old molecule in CKD and renal transplantation.

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Section: Hua and Renal Transplantationmentioning

confidence: 99%

Hyperuricemia and chronic kidney disease: an enigma yet to be solved

et al. 2014

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“…This is in accordance with Armstrong et al 45 , who found an inverse relationship between baseline uric acid and eGFR in 90 renal transplant recipients. However Gores et al studying 262 patients found severely hyperuricemic cases had a mean Creatinine similar to those with normal uric acid 46 . There are also several studies that shows that increase uric acid is a major risk factor for cardiovascular disease, kidney disease, pregnancy related complications and concomitant mortality 47,48 .…”

Section: Discussionmentioning

confidence: 95%

A retrospective study of hyperurecemia in renal transplant recipients

Baruah

Datta

Nath

et al. 2014

Int Jour of Biomed Res

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“…17 Kidney allograft recipients have as high as 84% increased prevalence of hyperuricemia than people in the general population. 5,6 Several factors contribute to the high prevalence of hyperuricemia in kidney transplant recipients including hypertension and use of diuretics and calcineurin inhibitors. Kidney transplant has no direct effect on uric acid excretion; this was shown in studies of uric acid metabolism in kidney transplant recipients before cyclosporine therapy was developed.…”

Section: Discussionmentioning

confidence: 99%

“…Hyperuricemia is associated with the progression of chronic kidney disease (CKD), hypertension, and cardiovascular disease in kidney transplant recipients. [1][2][3][4][5][6][7] Uric acid is an independent risk factor for the development of functional decline of kidney allografts and chronic allograft nephropathy. Uric acid may cause kidney damage because uric acid impairs endothelial cell function, stimulates vascular smooth muscle cell proliferation, increases inflammatory markers, and activates the reninangiotensin system.…”

Section: Introductionmentioning

confidence: 99%

Untitled

2014

Exp Clin Transplant

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Objectives: Hyperuricemia may be a risk factor for graft loss in kidney transplant recipients. The purpose of this study was to evaluate the effects of allopurinol in kidney transplant recipients. Materials and Methods: A single center retrospective case-control study was performed with kidney transplant recipients who were treated with allopurinol (54 patients) and a control group matched for time of transplant (± 3 months) and estimated glomerular filtration rate (54 patients). We evaluated the relation between allopurinol use and estimated glomerular filtration rate, graft survival, blood pressure, and number of antihypertensive drugs used. Results: At the start of allopurinol therapy, mean serum uric acid level was greater in the allopurinol (476 ± 119 μmol/L) than control group (404 ± 125 μmol/L; P ≤ .001) and estimated glomerular filtration rate was similar between the 2 groups (allopurinol, 39 ± 16 mL/min; control, 38 ± 16 mL/min; not significant). At 1 year, mean estimated glomerular filtration rate was greater in the allopurinol than control group (allopurinol, 41 ± 15 mL/min; control, 36 ± 13 mL/min; P ≤ .04). At 2 years, mean serum uric acid level was significantly lower in the allopurinol (399 ± 101 μmol/L) than control group (452 ± 95 μmol/L; P ≤ .02). Graft survival, blood pressure, and antihypertensive requirements were similar between the groups. Conclusions: Allopurinol use is associated with preservation of estimated glomerular filtration rate in kidney transplant recipients. There may be potential benefit in treating asymptomatic hyperuricemia in kidney transplant recipients.

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Hyperuricemia after renal transplantation

Cited by 73 publications

References 11 publications

Hyperuricemia and chronic kidney disease: an enigma yet to be solved

Hyperuricemia and chronic kidney disease: an enigma yet to be solved

A retrospective study of hyperurecemia in renal transplant recipients

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