Meta-analysis on allopurinol preventive intervention on contrast-induced acute kidney injury with random controlled trials

Abstract

Objectives: The objective of this meta-analysis on randomized controlled trials is to evaluate whether the administration of allopurinol with or without hydration will reduce contrast-induced acute kidney injury (CI-AKI) in patients undergoing contrast exposure. Background: The efficacy of allopurinol in the prevention of CI-AKI after cardiac catheterization and percutaneous coronary intervention (PCI) is significantly related to the heterogeneous results. Methods: Two investigators independently searched MEDLINE, EMBASE, the Cochrane Controlled Trials Registry, the China Wanfang Data, the China Biological Medicine Database and the China National Knowledge Infrastructure (CNKI) databases for randomized controlled trials (RCTs) comparing allopurinol with placebo or no allopurinol for the prevention of CI-AKI in patients from their inception to July 31, 2018. The primary outcome was the incidence of CI-AKI, and the secondary outcomes were the differences of serum creatinine (Scr), blood urea nitrogen (BUN), uric acid (UA), and estimated glomerular filtration rate (eGFR) levels between groups after contrast media exposure. We used fixed-effects or random-effects models according to I 2 statistics. The meta-analytic procedures were completed by Review Manager, version 5.3. Achievements: Eight random controlled trials with 1141 patients were included for this analysis. Compared with the control, allopurinol was associated with a reduced risk of CI-AKI (Relatives Risk (RR) 0.39, 95% confidence interval [CI] 0.20,0.74, P = .004) and only a intend for decrease a post-procedure uric acid levels compared with the controlled ones at 48 hours (standardized mean difference (SMD) −0.72, 95% CI −1.44, 0.01, P = .05). But the difference of post-procedure uric acid levels was not statistically significant in allopurinol groups compared with controlled groups. There were lower post-procedure Scr and BUN levels in allopurinol groups than those in controlled groups (SMD −0.50, 95% CI −0.79,−0.21, P = .0009; SMD −0.40, 95% CI −0.60,−0.20, P < .0001;respectively). There were higher post-procedure eGFR levels in allopurinol groups than those in controlled groups (SMD 0.65, 95% CI 0.48, 0.83, P < .0001). Conclusion: The main findings of this meta-analysis are focus on allopurinol may cause reduces in the incidence of CI-AKI in patients undergoing interventional coronary procedures. Further researches are still required for confirmation.

Efficacy and safety of urate-lowering agents in asymptomatic hyperuricemia: systematic review and network meta-analysis of randomized controlled trials

“…The treatment effects observed between high-and low-dose ULTs were not significantly different and a sensitivity analysis that excluded rasburicase still showed significantly lower composite renal events from allopurinol and febuxostat compared to placebo/no ULT controls (Additional file: Table S10 and Table S11). Our findings suggest that allopurinol and febuxostat can reduce further composite renal events and slow progression of CKD, supporting previous studies for allopurinol [37][38][39][40] and febuxostat [22,27,28,41,42].…”

Febuxostat combined with hydration for the prevention of contrast-induced nephropathy in hyperuricemia patients undergoing percutaneous coronary intervention

“…Allopurinol may have a direct protective effect on endothelial cells and simultaneously improve renal medullary perfusion, thus counterbalancing the direct and ischemic effects induced by the contrast medium, and allopurinol may reduce the incidence of contrast-induced acute kidney injury in patients undergoing interventional coronary procedures. [18] Febuxostat, structurally difering from allopurinol, is a novel selective xanthine oxidase inhibitor, which is metabolized by the liver and excreted via both urine and feces. [19] Febuxostat has a renoprotective effect in patients with chronic kidney disease.…”

“…Oxidative stress is an important factor involved in endothelial dysfunction and ischemia-reperfusion injury and may be implicated in the pathogenesis of CIN. Allopurinol may have a direct protective effect on endothelial cells and simultaneously improve renal medullary perfusion, thus counterbalancing the direct and ischemic effects induced by the contrast medium, and allopurinol may reduce the incidence of contrast-induced acute kidney injury in patients undergoing interventional coronary procedures [18] …”

Comparing Trimetazidine with Allopurinol in Prevention of Contrast Induced Nephropathy After Coronary Angiography

“…These data suggest that trimetazidine may be beneficial in reducing CIN if given in the dose of 35 mg twice 48 h especially in patients with chronic kidney disease undergoing elective angiography. On the other hand, Ma et al showed in a meta-analysis of 8 studies (1141patients) significant reduction in CIN in patients who received allopurinol before exposure to contrast media [ 14 ]. Ghelich Khan et al study did not show a significant reduction in CIN in allopurinol groups (102 patients) versus the control group (108 patients) with 600 mg of allopurinol being given 24 h before elective PCI [ 15 ].…”