Uric Acid and Chronic Kidney Disease: New Understanding of an Old Problem

Kang, Duk Hee; Chen, Wei

doi:10.1016/j.semnephrol.2011.08.009

Cited by 82 publications

(86 citation statements)

References 62 publications

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“…All of these events may lead to renal fibrosis. 17 In this study, we found that lower glomerular filtration rates and higher serum creatinine concentrations, and cystatin C were associated with higher uric acid levels.…”

Section: Discussionmentioning

confidence: 53%

Hyperuricemia in Pediatric Renal Transplant Recipients

Gökçeoğlu

Akman²,

Koyun³

et al. 2013

Exp Clin Transplant

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Objectives: We sought to evaluate the prevalence and confounding clinical variables of hyperuricemia in pediatric kidney transplant patients. Materials and Methods:We retrospectively evaluated the medical records of 151 pediatric renal transplant recipients who received their grafts at Akdeniz University Medical Faculty in Antalya, Turkey, with a follow-up longer than 6 months. This retrospective, single-center study included 117 pediatric renal transplant recipients, after we had excluded the patients with changes in immunosuppressive treatment and graft loss, who were receiving therapy with allopurinol and furosemide. Patient information and laboratory data were obtained from patient charts and an electronic hospital database. Results: Mean uric acid levels of patients were 311 ± 74 μmol/L, and 24 of all of the patients (20%) had high uric acid levels. Fifteen patients taking tacrolimus (16%), and 9 of patients taking cyclosporine (39%) had hyperuricemia. The hyperuricemia rate of patients taking cyclosporine was significantly higher than it was for those patients taking tacrolimus (P = .014). Mean levels of uric acid in patients taking cyclosporine were higher than those of patients taking tacrolimus (344 ± 62 µmol/L and 303 ± 75 μmol/L; P = .006). There was a significant positive correlation between mean uric acid concentrations, and both serum creatinine (P = .000; r=0.487) and cystatin C (P = .000; r=0.433). There was negative correlation between mean uric acid concentration and estimated glomerular filtration rate (P = .000; r=-0.417). Mean uric acid levels of patients with intact graft function (estimated glomerular filtration rate ≥ 60 mL/min/1.73 m 2 ) was lower than the patients with a low estimated glomerular filtration rate (291 ± 67 μmol/L and 353 ± 71 μmol/L; P = .000). Mean uric acid level of patients with normal body mass index was significantly lower than that of patients who were obese-overweight (301 ± 64 μmol/L vs 343 ± 94 μmol/L; P = .045). Conclusions: We found 20% of our patient group had high uric acid levels. We also found that lower glomerular filtration rate, higher serum creatinine, cystatin c, obesity, and being overweight were risk factors for hyperuricemia in pediatric renal transplant recipients.

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Section: Discussionmentioning

confidence: 53%

Hyperuricemia in Pediatric Renal Transplant Recipients

Gökçeoğlu

Akman²,

Koyun³

et al. 2013

Exp Clin Transplant

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“…These events lead to renal fibrosis, and fibrosis is associated with a decrease in GFR. 3,6,9,10 Elimination of uric acid becomes less efficient with increasing kidney dysfunction. 2,5,11,12 Our study findings demonstrate a significant negative correlation between hyperuricemia and GFR.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 In most studies, serum uric acid level was a marker of renal dysfunction. [2][3][4][5][6] However, hyperuricemia occurs early after transplant and is associated with use of diuretics, cyclosporine therapy, a history of hyperuricemia, and decreased glomerular filtration rate (GFR). 1,3,5,7,8 The effect of hyperuricemia after kidney transplant on graft outcome has not been fully established, but a small number of studies have suggested that an increased serum uric acid level is a prognostic factor for the development of renal allograft impairment.…”

Section: Introductionmentioning

confidence: 99%

Untitled

2015

Exp Clin Transplant

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Objectives: Hyperuricemia is common in pediatric renal transplant recipients, and it is associated with poor allograft outcomes. Hyperuricemia occurs early after transplant and is associated with use of diuretics, cyclosporine therapy, a history of hyperuricemia, and decreased glomerular filtration rate. We aimed to investigate causes and effects of hyperuricemia on allograft outcomes in our patients. Materials and Methods: There were 81 pediatric transplant patients (41 female and 40 male) included in the study. Demographic characteristics and laboratory parameters were recorded. Risk factors for hyperuricemia and the effects of plasma uric acid levels at 3, 6, 12, and 36 months on allograft outcomes were evaluated. Results: Mean age was 16.9 ± 5.6 years. Mean follow-up after transplant was 3.5 ± 0.47 years. Hyperuricemia was detected in 17.6% patients. A significant negative correlation was observed between 6-month uric acid level and 36-month glomerular filtration rate (r = -0.33, P = .04; r = -0.33, P = .017). A significant positive correlation between 3-and 6-month uric acid levels and 36-month plasma creatinine level was observed (r = -0.44, P = .01; r = -0.51, P = .001). There was no significant correlation between plasma uric acid level and body mass index, plasma lipid levels, use of diuretics, or immunosuppressive treatment (tacrolimus or cyclosporine). Conclusions: Uric acid levels may have predictive value in the long-term assessment of renal function. Posttransplant hyperuricemia can be used as a longterm prognostic marker of poor renal outcome. Patients with hyperuricemia should be monitored closely for renal function.

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“…U cilju bezbednosti primene alopurinola (smanjenje rizika od sindroma preosetljivosti na alopurinol), početna doza alopurinola ne treba da bude veća od 1,5mg/ml/min/1,73m 2 Komplijantnost bolesnika (redovno uzimanje alopurinola) se procenjuje merenjem koncentracije oksipurinola u serumu. Koncentracija oksipurinola u serumu manja od 20mol/l ukazuje na neredovno uzimanje alopurinola (odsustvo komplijantnosti bolesnika).…”

Section: Lečenje Hiperurikemije Lečenje Simptomatske Hiperurikemijeunclassified

“…Incidencija ovog sindroma iznosi 0,1%, a glavni faktori rizika za njegov nastanak su: početna doza alopurinola ≥1,5mg/ml/min/1,73m 2 , ukupna doza alopurinola ≥300mg/dan (kod 7% bolesnika dolazi do razvoja AHS-a), oštećenje bubrega (bolesnici sa oštećenom funkcijom bubrega imaju 3-4 puta veći rizik od razvoja AHS-a, u odnosu na bolesnike sa normalnom funkcijom bubrega), upotreba diuretika (furosemid, tiazidni diuretici), HLA B58 25-29. Stopa smrtnosti povezane sa sindromom preosetljivosti na alopurinol iznosi 27%.…”

Section: Lečenje Hiperurikemije Lečenje Simptomatske Hiperurikemijeunclassified