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Serum uric acid and risk for acute kidney injury following contrast: an evaluation of epidemiology, clinical trials, and potential mechanisms

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SCHOOL OF MEDICINE
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Solak, Yalcin
Afsar, Baris
Nistor, Ionut
Aslan, Gamze
Donciu, Mihaela-Dora
Lanaspa, Miguel A.
Ejaz, Ahsan A.
Johnson, Richard J.
Covic, Adrian

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Abstract

Contrast-induced acute kidney injury (CI-AKI) is a common cause of hospital-acquired acute kidney injury (AKI). We evaluated the evidence that uric acid (UA) plays a pathogenic role in CI-AKI. Ten studies were eligible for inclusion for meta-analysis. Hyperuricemia predicted risk for cases with AKI in prospective cohort studies. Higher levels of serum UA (SUA), as defined by the authors, were associated with a 2-fold increased risk to develop AKI (pooled odds ratio 2.03; 95% confidence interval [CI] 1.48-2.78). Significant heterogeneity was found in cohort studies (P = .001, I-2 = 85.7%). In 2 clinical trials, lowering of SUA with saline hydration was significantly associated with reduced risk for AKI compared with saline hydration alone or saline hydration with N-acetyl cysteine. An analysis of 2 randomized controlled trials found that allopurinol with saline hydration had a significant protective effect on renal function (assessed by serum creatinine values) compared with hydration alone (mean difference: -0.52 mg/dL; 95% CI: -0.81 to -0.22). Hyperuricemia independently predicts CI-AKI. Two clinical trials suggest lowering SUA may prevent CI-AKI. The mechanism by which UA induces CI-AKI is likely related to acute uricosuria.

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Sage

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Peripheral vascular disease, Cardiovascular system, Cardiology

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Angiology

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10.1177/0003319716644395

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