Efficacy of allopurinol pretreatment for prevention of contrast-induced nephropathy: a randomized controlled trial

Erol, Tansel; Tekin, Abdullah; Katırcıbaşı, Mahmut Tuna; Sezgin, Nurzen; Bilgi, Muhammet; Tekin, Göknur; Zümrütdal, Ayşegül; Sezgin, Atilla; Müderrisoğlu, Haldun

doi:10.1016/j.ijcard.2012.04.068

Cited by 47 publications

(51 citation statements)

References 31 publications

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“…CIN is detected in up to 50% of patients with pre-existing renal impairment and diabetic nephropathy and less than 2% of patients with normal renal function (39,40). A randomized controlled clinical trial by Erol et al, in 2013, described the effectiveness of allopurinol pretreatment for prevention of CIN.…”

Section: Allopurinol and Nephrotoxicitymentioning

confidence: 99%

“…In the allopurinol group, they showed that median serum creatinine concentration decreased significantly 4 days after radio contrast administration. On the other hand, allopurinol along with hydration reduced the prevalence of CIN in individuals with impaired kidney function (39). In another report in 2014, the patients received either of 3 drugs including saline hydration (1 mL/kg/h), allopurinol (300 mg/d) and N-acetylcysteine (600 mg bid) 12 hours before and after administration of contrast agent.…”

Section: Allopurinol and Nephrotoxicitymentioning

confidence: 99%

See 1 more Smart Citation

An update on allopurinol and kidney failure; new trend for an old drug

Alirezaei¹,

Argani²,

Asgharpour³

et al. 2017

J Renal Inj Prev

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Findings of this review show that treatment with allopurinol as a purine inhibitor of xanthine oxidase enzyme can decrease oxidative stress and uric acid levels and may help to restore the endothelial function and slow down the progression of renal disorder to end stage renal disease. Allopurinol is an inhibitor of xanthine oxidase (XO) enzyme. This drug is a reducer of uric acid in the body and one of the golden drugs with worldwide administration. XO is an important biological source of free radical generation. Allopurinol as an antioxidant, has direct and indirect antioxidant activity on these free radicals such as hydroxyl radical and superoxide anion. The purpose of this paper is to determine the impact of allopurinol on some aspects of renal disturbances such as renal ischemia/reperfusion injury (IRI), nephrotoxicity and contrast-induced nephropathy (CIN). Please cite this paper as:

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Section: Allopurinol and Nephrotoxicitymentioning

confidence: 99%

Section: Allopurinol and Nephrotoxicitymentioning

confidence: 99%

An update on allopurinol and kidney failure; new trend for an old drug

Alirezaei¹,

Argani²,

Asgharpour³

et al. 2017

J Renal Inj Prev

View full text Add to dashboard Cite

show abstract

“…Two trials have focused on uratelowering therapy in the perioperative setting in patients undergoing vascular and cardiothoracic surgery, with some potential benefit in late postsurgical outcomes and in GFR [69,70]. Another randomized trial of allopurinol in addition to hydration found a significant reduction in contrast-induced nephropathy in patients undergoing heart catheterization [71]. One open-label randomized trial of allopurinol in 54 patients with CKD stage III or proteinuria 90.5 g/day found a significant slowing of progression of CKD in patients on allopurinol at the end of 12 months, with 16 % in the allopurinol arm versus 46 % of control patients experiencing a 940 % decrease in baseline GFR [72].…”

Section: The Impact Of Urate-lowering Therapy On Clinical Outcomesmentioning

confidence: 99%

Gout and Hyperuricemia—Serious Risk Factors for Morbidity and Mortality or Just Indicators of “The Good Life”—The Evidence to Date

Fernández

Markenson

2015

Curr Treat Options in Rheum

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Gout and hyperuricemia are associated with cardiovascular disease and its major risk factors and even more closely with chronic kidney disease. The preponderance of results from observational cohorts demonstrate that gout and hyperuricemia are associated with an increased risk of cardiovascular disease and chronic kidney disease that is independent of other factors, though that increase is of a smaller magnitude than that seen with traditional risk factors. In some studies, the relative increase in risk associated with elevated uric acid is more pronounced in women than in men. We have interpreted these results as a prompt to be more aggressive in screening our gout patients for modifiable cardiovascular risk factors and chronic kidney disease and reducing those risks as much as possible through lifestyle changes, modifications to diet, and medications. Many gout patients have indications for urate-lowering therapy related to their disease, so the dilemma of whether to initiate treatment is not present. There has not yet been sufficient demonstration in randomized controlled trials of benefit from urate-lowering therapies in patients with asymptomatic hyperuricemia with regard to cardiovascular or renal outcomes. However, there are intriguing preliminary results in several studies that may demonstrate a specific benefit of allopurinol or febuxostat in certain populations.

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“…A recent meta-analysis conducted by our group 3 concluded that an elevated SUA level is a risk factor for the development of CI-AKI. In addition, 2 clinical trials, 4,5 discussed in this meta-analysis, suggested that lowering SUA levels with allopurinol may prevent CI-AKI. We therefore speculate that SUA is an independent risk factor for CI-AKI.…”

mentioning

confidence: 96%

Reply to: Uric Acid and Contrast-Induced Nephropathy: Diagnostic Marker, Therapeutic Target, or Innocent Bystander?

Sahan

Kanbay

2017

Angiology

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We thank Canpolat and colleagues 1 for their interest in our paper. 2 Firstly, they 1 mention that the SYNTAX score was not calculated in our study. 2 This valuable comment warrants consideration in future studies.Secondly, the authors 1 requested a comment on whether serum uric acid (SUA) level in the development of contrastinduced acute kidney injury (CI-AKI) was a diagnostic marker or an innocent bystander. A recent meta-analysis conducted by our group 3 concluded that an elevated SUA level is a risk factor for the development of CI-AKI. In addition, 2 clinical trials, 4,5 discussed in this meta-analysis, suggested that lowering SUA levels with allopurinol may prevent CI-AKI. We therefore speculate that SUA is an independent risk factor for CI-AKI. Postulated mechanisms include that SUA may increase oxidative stress as well as activate cytokines and inflammation, which leads to endothelial dysfunction, reduced renal blood flow, increased renal vascular resistance, and may cause crystallization and tubular luminal obstruction. Therefore, SUA may be an independent player in the pathogenesis of CI-AKI. 6 Thirdly, the authors 1 enquired regarding the subtypes of statin therapy used. Unfortunately, details with respect to dose and type of statins were unavailable in the records. Consequently, we were unable to carry out a subanalysis of statin therapy, and this is a limitation of our study. 2 In our study, 2 we included well-known established risk factors for the development of contrast-induced nephropathy (CIN) in multivariate analysis to show independent associations between CIN and SUA. In conclusion, the findings of our study, and previous studies, may help understand the pathophysiology of CI-AKI and identify novel strategies for preventing CI-AKI.

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Efficacy of allopurinol pretreatment for prevention of contrast-induced nephropathy: a randomized controlled trial

Cited by 47 publications

References 31 publications

An update on allopurinol and kidney failure; new trend for an old drug

An update on allopurinol and kidney failure; new trend for an old drug

Gout and Hyperuricemia—Serious Risk Factors for Morbidity and Mortality or Just Indicators of “The Good Life”—The Evidence to Date

Reply to: Uric Acid and Contrast-Induced Nephropathy: Diagnostic Marker, Therapeutic Target, or Innocent Bystander?

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