Researcher:
Aykanat, Aslı

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Undergraduate Student

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Aslı

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Aykanat

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Aykanat, Aslı

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20171

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Researcher Of Publications: search.filters.isAuthorOfPublication.72945f97-79ef-47e6-b3f3-3aecad0463e8

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    Serum uric acid and risk for acute kidney injury following contrast: an evaluation of epidemiology, clinical trials, and potential mechanisms
    (Sage, 2017) Solak, Yalcin; Afsar, Baris; Nistor, Ionut; Aslan, Gamze; Donciu, Mihaela-Dora; Lanaspa, Miguel A.; Ejaz, Ahsan A.; Johnson, Richard J.; Covic, Adrian; N/A; Kanbay, Mehmet; Aykanat, Aslı; Bozlak, Özlem Hilal Çağlayan; Faculty Member; Undergraduate Student; Undergraduate Student; School of Medicine; School of Medicine; School of Medicine; 0000-0002-1297-0675; N/A; N/A
    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.